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1.  Mortality and Exposure Response among 14,458 Electrical Capacitor Manufacturing Workers Exposed to Polychlorinated Biphenyls (PCBs) 
Environmental Health Perspectives  2006;114(10):1508-1514.
Background
We expanded an existing cohort of workers (n = 2,588) considered highly exposed to polychlorinated biphenyls (PCBs) at two capacitor manufacturing plants to include all workers with at least 90 days of potential PCB exposure during 1939–1977 (n = 14,458). Causes of death of a priori interest included liver and rectal cancers, previously reported for the original cohort, and non-Hodgkin lymphoma (NHL), melanoma, and breast, brain, intestine, stomach, and prostate cancers, based on other studies.
Methods
We ascertained vital status of the workers through 1998, and cumulative PCB exposure was estimated using a new job exposure matrix. Analyses employed standardized mortality ratios (SMRs; U.S., state, and county referents) and Poisson regression modeling.
Results
Mortality from NHL, melanoma, and rectal, breast, and brain cancers were neither in excess nor associated with cumulative exposure. Mortality was not elevated for liver cancer [21 deaths; SMR 0.89; 95% confidence interval (CI), 0.55–1.36], but increased with cumulative exposure (trend p-value = 0.071). Among men, stomach cancer mortality was elevated (24 deaths; SMR 1.53; 95% CI, 0.98–2.28) and increased with cumulative exposure (trend p-value = 0.039). Among women, intestinal cancer mortality was elevated (67 deaths; SMR 1.31; 95% CI, 1.02–1.66), especially in higher cumulative exposure categories, but without a clear trend. Prostate cancer mortality, which was not elevated (34 deaths; SMR 1.04; 95% CI, 0.72–1.45), increased with cumulative exposure (trend p-value = 0.0001).
Conclusions
This study corroborates previous studies showing increased liver cancer mortality, but we cannot clearly associate rectal, stomach, and intestinal cancers with PCB exposure. This is the first PCB cohort showing a strong exposure–response relationship for prostate cancer mortality.
doi:10.1289/ehp.9175
PMCID: PMC1626402  PMID: 17035134
cancer; electrical capacitor manufacturing; liver cancer; mortality; occupational exposure; PCBs; polychlorinated biphenyls; prostate cancer
2.  Reduced Antibody Responses to Vaccinations in Children Exposed to Polychlorinated Biphenyls 
PLoS Medicine  2006;3(8):e311.
Background
Developmental exposure to polychlorinated biphenyls (PCBs) has been implicated as a possible cause of deficient immune function in children. This study was designed to assess whether prenatal and postnatal exposure to PCBs impacts on antibody response to childhood immunizations.
Methods and Findings
Two birth cohorts were formed in the Faroe Islands, where exposures vary widely, because traditional diets may include whale blubber contaminated with PCBs. Prenatal exposure was determined from maternal concentrations of PCBs in pregnancy serum and milk. Following routine childhood vaccinations against tetanus and diphtheria, 119 children were examined at 18 mo and 129 children at 7 y of age, and their serum samples were analyzed for tetanus and diphtheria toxoid antibodies and for PCBs. The antibody response to diphtheria toxoid decreased at age 18 mo by 24.4% (95% confidence interval [CI], 1.63–41.9; p = 0.04) for each doubling of the cumulative PCB exposure at the time of examination. The diphtheria response was lower at age 7 y and was not associated with the exposure. However, the tetanus toxoid antibody response was affected mainly at age 7 y, decreasing by 16.5% (95% CI, 1.51–29.3; p = 0.03) for each doubling of the prenatal exposure. Structural equation analysis showed that the early postnatal exposure was the most important predictor of a decreased vaccination response.
Conclusions
Increased perinatal exposure to PCBs may adversely impact on immune responses to childhood vaccinations. The clinical implications of insufficient antibody production emphasize the need for prevention of immunotoxicant exposures.
A study of two birth cohorts in the Faroe Islands, where diets may include whale blubber contaminated with polychlorinated biphenyls (PCBs), suggests exposure to PCBs may reduce immune response to childhood vaccinations.
Editors' Summary
Background.
These days, mothers are as likely to worry about potential side-effects of childhood vaccinations as about whether they completely protect their child against infections. But healthy children vary in how well vaccinations “take.” After tetanus and diphtheria vaccination, for example, some children produce large quantities of antibodies that protect them against these serious bacterial diseases; others make a weaker, sometimes inadequate, immune response. What causes this variation is unclear, but one possibility is that the developing immune system is damaged in some babies by exposure both before birth and after birth through breast milk to “immunotoxicants” such as polychlorinated biphenyls (PCBs). These stable, man-made chemicals, which were widely used last century as insulators in electrical equipment and as fire retardants, accumulate and persist in the environment where they affect animal and human health. PCB-exposed babies often have a small thymus (the gland where immune system cells mature), make decreased amounts of antibodies, and have more childhood infections.
Why Was This Study Done?
Given these observations, could exposure to PCBs be partly responsible for the variable immunological responses of children to vaccination? If it is, and if environmental PCB levels remain high, it might be necessary to adapt more intensive vaccination programs so that all children are adequately protected against infectious diseases. In this study, the researchers examined whether prenatal and postnatal exposure to PCBs affects antibody responses to childhood vaccinations
What Did the Researchers Do and Find?
The researchers enrolled two groups of children—one group born in 1994–1995, the other in 1999–2001—living on the Faroe Islands in the North Atlantic. Here, people are exposed to high levels of PCBs through eating contaminated whale blubber. All the children received routine vaccinations against diphtheria and tetanus. The bacteria that cause these illnesses do so by producing a “toxoid,” so a harmless quantity of these toxic proteins is injected to stimulate a protective antibody response. For the older group, a blood sample was taken when they were seven and half years old to test for antibodies against diphtheria and tetanus toxoids; for the younger group, a sample was taken at 18 months. The exposure of the children to PCBs was assessed by measuring PCBs in their mothers' blood during pregnancy, in their mothers' milk soon after birth, and in their own blood when their antibodies were tested. The researchers found that the antibody response to diphtheria toxoid in the younger group of children was reduced by nearly a quarter for every doubling in their total exposure to PCBs. The tetanus toxoid response in the older children was reduced by a similar amount by prenatal exposure to PCBs. Although most of the children made enough antibodies to both toxoids to provide protection, about a fifth of the older children—mainly those with the highest exposures to PCBs—had worryingly low levels of diphtheria toxoid antibodies.
What Do These Findings Mean?
These results reveal an association between exposure to PCBs, particularly soon after birth, and a reduction in immunoprotection after childhood vaccinations. It is not clear, however, exactly how big this effect may be. This is uncertain for two reasons. First, the estimates of how much antibody responses are reduced by doubling PCB exposure are imprecise—for the younger children this change in exposure might actually have very little effect on their response to diphtheria vaccination or it could halve their response. Second, the estimates of PCB exposures are based on only three samples of body fluids so provide only a crude indication of exposure. Nevertheless, these results in children exposed to high levels of PCBs indicate that the immune function of children might also be adversely affected by the lower levels of PCBs found elsewhere in the world. Although the changes in immune function are subtle, they could be clinically important, write the researchers, and might affect both the general health of children and the degree of protection against infectious diseases that vaccination provides. Finally, these findings suggest that efforts must be stepped up to reduce PCB exposure levels to protect the sensitive immune systems of young children from these potent immunotoxicants.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030311.
Tox Town, a Web site available from the US National Institutes of Health, provides an introduction to toxic chemicals and environmental health risks
US Agency for Toxic Substances and Disease Registry fact sheet on PCBs
US Environmental Protection Agency information on PCBs
MedlinePlus encyclopedia entries on immunization tetanus vaccine, and diphtheria vaccine
Wikipedia pages on PCBs and vaccines (note: Wikipedia is a free online encyclopedia that anyone can edit)
doi:10.1371/journal.pmed.0030311
PMCID: PMC1551916  PMID: 16942395
3.  Dietary exposure to polychlorinated biphenyls and dioxins from infancy until adulthood: A comparison between breast-feeding, toddler, and long-term exposure. 
Food is the major source for polychlorinated biphenyl (PCB) and dioxin accumulation in the human body. Therefore, investigating food habits from early ages until reproductive age (25 years) is important in order to assess exposure risk for the next generation. The objective of this study was to assess the PCB/dioxin exposure and the relative contribution of different foods to total exposure during preschool age. Particularly, the importance of lactational PCB/dioxin exposure vs. dietary exposure until adulthood was investigated. A cohort of 207 children was studied from birth until preschool age. Based on 3 planar PCBs and 17 2,3,7,8-substituted dibenzo-para-dioxins (PCDDs) and dibenzofurans (PCDFs) measured in breast milk, a model was developed to calculate the cumulative toxic equivalent (TEQ) intake during breast-feeding (0-1 year). In 3. 5-year-old children, daily dietary intake of planar PCB-TEQ and dioxin-TEQ was measured with a validated food questionnaire. Cumulative TEQ intake from 1 to 5 years was estimated using the PCB- and dioxin-TEQ intake measured with the food questionnaire. Cumulative TEQ intake from 6 to 25 years was estimated using national food consumption and contamination data of PCB- and dioxin-TEQ intake. In toddlers, dairy products contributed 43% to PCB-TEQ and 50% to dioxin-TEQ intake. Meat and meat products contributed 14% and 19%, respectively, and processed foods 23% and 15%, respectively. Breast-feeding for 6 months contributed to the cumulative PCB/dioxin TEQ intake until 25 years of age, 12% in boys and 14% in girls. The daily TEQ intake per kilogram body weight is 50 times higher in breast-fed infants and three times higher in toddlers than in adults. Long-term dietary exposure to PCBs and dioxins in men and women is partly due to breast-feeding (12 and 14%, respectively). After weaning, dairy products, processed foods, and meat are major contributors of PCB and dioxin accumulation until reproductive age. Instead of discouraging breast-feeding, maternal transfer of PCBs and dioxins to the next generation must be avoided by enforcement of strict regulations for PCB and dioxin discharge and by reducing consumption of animal products and processed foods in all ages.
Images
PMCID: PMC1566290  PMID: 9872716
4.  Update: cohort mortality study of workers highly exposed to polychlorinated biphenyls (PCBs) during the manufacture of electrical capacitors, 1940-1998 
Environmental Health  2006;5:13.
Background
The National Institute for Occupational Safety and Health previously reported mortality for a cohort of workers considered highly exposed to polychlorinated biphenyls (PCBs) between 1939 and 1977 at two electrical capacitor manufacturing plants. The current study updated vital status, examined liver and rectal cancer mortality previously reported in excess in this cohort and evaluated mortality from non-Hodgkin's lymphoma (NHL) and cancers of the stomach, intestine, breast, prostate, skin (melanoma) and brain reported to be in excess in other cohort and case-control studies of PCB-exposed persons.
Methods
Mortality was updated through 1998 for 2572 workers. Age-, gender-, race- and calendar year-adjusted standardized mortality ratios (SMRs) and 95% confidence intervals (CI) were calculated using U.S., state and county referent rates. SMRs using U.S. referent rates are reported. Duration of employment was used as a surrogate for exposure.
Results
Consistent with the previous follow-up, mortality from biliary passage, liver and gall bladder cancer was significantly elevated (11 deaths, SMR 2.11, CI 1.05 – 3.77), but mortality from rectal cancer was not (6 deaths, SMR 1.47, CI 0.54 – 3.21). Among women, mortality from intestinal cancer (24 deaths, SMR 1.89, CI 1.21 – 2.82) and from "other diseases of the nervous system and sense organs", which include Parkinson's disease and amyotrophic lateral sclerosis, (15 deaths, SMR 2.07, CI 1.16 – 3.42) were elevated. There were four ALS deaths, all women (SMR 4.35, CI 1.19–11.14). Mortality was elevated for myeloma (7 deaths, SMR 2.11, CI 0.84 – 4.34), particularly among workers employed 10 years or more (5 deaths, SMR 2.80, CI 0.91 – 6.54). No linear associations between mortality and duration of employment were observed for the cancers of interest.
Conclusion
This update found that the earlier reported excess in this cohort for biliary, liver and gall bladder cancer persisted with longer follow-up. Excess mortality for intestinal cancer among women was elevated across categories of duration of employment; myeloma mortality was highest among those working 10 years or more. The small numbers of deaths from liver and intestinal cancers, myeloma and nervous system diseases coupled with the lack of an exposure-response relationship with duration of employment preclude drawing definitive conclusions regarding PCB exposure and these causes of death.
doi:10.1186/1476-069X-5-13
PMCID: PMC1524943  PMID: 16716225
5.  Environmental Exposures and Puberty in Inner-City Girls 
Environmental research  2008;107(3):393-400.
Background
Hormonally active environmental exposures are suspected to alter onset of puberty in girls, but research on this question has been very limited.
Objective
We investigated pubertal status in relation to hormonally active environmental exposures among a multiethnic group of 192 healthy nine-year old girls residing in New York City.
Methods
Information was collected on breast and pubic hair stages, weight and height. Phytoestrogen intake was estimated from a food frequency questionnaire. Three phytoestrogens and bis-phenolA (BPA) were measured in urine. In a subset, 1,1′-dichloro-2,2′-bis(4-chlorophenyl)ethylene (DDE), polychlorinated biphenyls (PCBs) were measured in blood plasma and lead (Pb) in blood. Associations of exposures with pubertal stages (present=stage 2+ vs absent=stage 1) were examined using t-tests and Poisson multivariate regression to derive prevalence ratios (PR, 95%-confidence limits [CI]).
Results
Breast development was present in 53% of girls. DDE, Pb, and dietary intakes of phytoestrogens were not significantly associated with breast stage. Urinary phytoestrogen biomarker concentrations were lower among girls with breast development than with no development. In multivariate models, main effects were strongest for two urinary isoflavones, daidzein (PR 0.89 [0.83-0.96] per ln-μg/g creatinine) and genistein (0.94 [0.88-1.01]). Body mass index (BMI) is a hormonally relevant, strong risk factor for breast development. Therefore, BMI-modification of exposure effects was examined, and associations became stronger. Delayed breast development was observed among girls with below-median BMI and 3rd tertile (high exposure) of urinary daidzein (PR 0.46 [0.26-0.78]); a similar effect was seen with genistein, comparing to girls ≥median BMI and lowest two tertiles (combined) of these isoflavones. With urinary enterolactone a phytoestrogen effect was seen only among girls with high BMI, where breast development was delayed among those with high urinary enterolactone (PR 0.55 [0.32 - 0.96] for the upper tertile vs lower two combined). There was no main effect of PCBs on breast stage, but girls with below-median BMI and ≥median PCB levels had reduced risk for breast development (any vs none) compared with other BMI-PCB groups. No biomarkers were associated with hair development, which was present in 31% of girls.
Conclusions
Phytoestrogens and PCBs are environmental exposures that may delay breast development, especially in conjunction with BMI which governs the endogenous hormonal milieu. Further research to confirm these findings may improve our understanding of the role of early-life development in breast cancer risk and other chronic diseases related to obesity.
doi:10.1016/j.envres.2008.03.006
PMCID: PMC3974622  PMID: 18479682
puberty; environment; biomarkers; BMI; phytoestrogen; DDE; PCB; diet
6.  Cancer mortality among electric utility workers exposed to polychlorinated biphenyls. 
OBJECTIVES: To assess whether excess mortality from cancer, malignant melanoma of the skin, and cancers of the brain and liver in particular, is associated with long term occupational exposure to polychlorinated biphenyls (PCBs). METHODS: An epidemiological study of mortality was conducted among 138,905 men employed for at least six months between 1950 and 1986 at five electrical power companies in the United States. Exposures were assessed by panels composed of workers, hygienists, and managers at each company, who considered tasks performed by workers in 28 job categories and estimated weekly exposures in hours for each job. Poisson regression was used to examine mortality in relation to exposure to electrical insulating fluids containing PCBs, controlling for demographic and occupational factors. RESULTS: Neither all cause nor total cancer mortality was related to cumulative exposure to PCB insulating fluids. Mortality from malignant melanoma increased with exposure; rate ratios (RRs) relative to unexposed men for melanoma were 1.23 (95% confidence interval (95% CI) 0.56 to 2.52), 1.71 (0.68 to 4.28) and 1.93 (0.52 to 7.14) for men with < 2000, > 2000-10,000, and > 10,000 hours of cumulative exposure to PCB insulating fluids, respectively, without consideration of latency. Lagging exposure by 20 years yielded RRs of 1.29 (0.76 to 2.18), 2.56 (1.09 to 5.97), and 4.81 (1.49 to 15.50) for the same exposure levels. Mortality from brain cancer was modestly increased among men with < 2000 hours (RR 1.61, 95% CI 0.86 to 3.01) and > 2000-10,000 hours exposure (RR 1.79, 95% CI 0.81 to 3.95), but there were no deaths from brain cancer among the most highly exposed men. A lag of five years yielded slightly increased RRs. Mortality from liver cancer was not associated with exposure to PCB insulating fluids. CONCLUSIONS: This study was larger and provided more detailed information on exposure than past investigations of workers exposed to PCBs. The results suggest that PCBs cause cancer, with malignant melanoma being of particular concern in this industry.
PMCID: PMC1128926  PMID: 9404319
7.  Mortality among Workers Exposed to Polychlorinated Biphenyls (PCBs) in an Electrical Capacitor Manufacturing Plant in Indiana: An Update 
An Indiana capacitor-manufacturing cohort (n = 3,569) was exposed to polychlorinated biphenyls (PCBs) from 1957 to 1977. The original study of mortality through 1984 found excess melanoma and brain cancer; other studies of PCB-exposed individuals have found excess non-Hodgkin lymphoma and rectal, liver, biliary tract, and gallbladder cancer. Mortality was updated through 1998. Analyses have included standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) using rates for Indiana and the United States, standardized rate ratios (SRRs), and Poisson regression rate ratios (RRs). Estimated cumulative exposure calculations used a new job–exposure matrix. Mortality overall was reduced (547 deaths; SMR, 0.81; 95% CI, 0.7–0.9). Non-Hodgkin lymphoma mortality was elevated (9 deaths; SMR, 1.23; 95% CI, 0.6–2.3). Melanoma remained in excess (9 deaths; SMR, 2.43; 95% CI, 1.1–4.6), especially in the lowest tertile of estimated cumulative exposure (5 deaths; SMR, 3.72; 95% CI, 1.2–8.7). Seven of the 12 brain cancer deaths (SMR, 1.91; 95% CI, 1.0–3.3) occurred after the original study. Brain cancer mortality increased with exposure (in the highest tertile, 5 deaths; SMR, 2.71; 95% CI, 0.9–6.3); the SRR dose–response trend was significant (p = 0.016). Among those working ≥90 days, both melanoma (8 deaths; SMR, 2.66; 95% CI, 1.1–5.2) and brain cancer (11 deaths; SMR, 2.12; 95% CI, 1.1–3.8) were elevated, especially for women: melanoma, 3 deaths (SMR, 5.99; 95% CI, 1.2–17.5); brain cancer, 3 deaths (SMR, 2.87; 95% CI, 0.6–8.4). These findings of excess melanoma and brain cancer mortality confirm results of the original study. Melanoma mortality was not associated with estimated cumulative exposure. Brain cancer mortality did not demonstrate a clear dose–response relationship with estimated cumulative exposure.
doi:10.1289/ehp.8253
PMCID: PMC1332650  PMID: 16393652
cancer; cohort study; exposure assessment; occupational exposure; polychlorinated biphenyls
8.  Exposure to polychlorinated biphenyl (PCB) congeners measured shortly after giving birth and subsequent risk of maternal breast cancer before age 50 
Discrete windows of susceptibility to toxicants have been identified for the breast, including in utero, puberty, pregnancy, and postpartum. We tested the hypothesis that polychlorinated biphenyls (PCBs) measured during the early postpartum predict increased risk of maternal breast cancer diagnosed before age 50. We analyzed archived early postpartum serum samples collected from 1959 to 1967, an average of 17 years before diagnosis (mean diagnosis age 43 years) for 16 PCB congeners in a nested case–control study in the Child Health and Development Studies cohort (N = 112 cases matched to controls on birth year). We used conditional logistic regression to adjust for lipids, race, year, lactation, and body mass. We observed strong breast cancer associations with three congeners. PCB 167 was associated with a lower risk (odds ratio (OR), 75th vs. 25th percentile = 0.2, 95 % confidence interval (95 % CI) 0.1, 0.8) as was PCB 187 (OR, 75th vs. 25th percentile = 0.4, 95 % CI 0.1, 1.1). In contrast, PCB 203 was associated with a sixfold increased risk (OR, 75th vs. 25th percentile = 6.3, 95 % CI 1.9, 21.7). The net association of PCB exposure, estimated by a post-hoc score, was nearly a threefold increase in risk (OR, 75th vs. 25th percentile = 2.8, 95 % CI 1.1, 7.1) among women with a higher proportion of PCB 203 in relation to the sum of PCBs 167 and 187. Postpartum PCB exposure likely also represents pregnancy exposure, and may predict increased risk for early breast cancer depending on the mixture that represents internal dose. It remains unclear whether individual differences in exposure, response to exposure, or both explain risk patterns observed.
doi:10.1007/s10549-012-2257-4
PMCID: PMC3473187  PMID: 23053646
PCBs; Polychlorinated biphenyls; Breast cancer; Pregnancy; Postpartum; Prospective; Human
9.  High breast milk levels of polychlorinated biphenyls (PCBs) among four women living adjacent to a PCB-contaminated waste site. 
Environmental Health Perspectives  1998;106(8):513-518.
As a consequence of contamination by effluents from local electronics manufacturing facilities, the New Bedford Harbor and estuary in southeastern Massachusetts is among the sites in the United States that are considered the most highly contaminated by polychlorinated biphenyls (PCBs). Since 1993, measures of intrauterine PCB exposure have been obtained for a sample of New Bedford area infants. Among 122 mother-infant pairs, we identified four milk samples with total PCB levels that were significantly higher than the rest, with estimated total PCBs ranging from 1,100 to 2,400 ng/g milk fat compared with an overall mean of 320 ng/g milk fat for the 122 women. The congener profile and history of one case was consistent with past occupational PCB exposures. Otherwise, the source of PCB exposures in these cases was difficult to specify. Environmental exposures including those from fish consumption were likely, whereas residence adjacent to a PCB-contaminated site was considered an unlikely exposure source. In all four cases, the infants were full-term, healthy newborns. Because the developing nervous system is believed to be particularly susceptible to PCBs (for example, prenatal PCB exposures have been associated with prematurity, decrements in birth weight and gestation time, and behavioral and developmental deficits in later infancy and childhood, including decrements in IQ), it is critical to ascertain if breast-feeding is a health risk for the women's infants. Despite the potential for large postnatal PCB exposures via breast milk, there is limited evidence of significant developmental toxicity associated with the transmission of moderate PCB concentrations through breast milk. Breast-feeding is associated with substantial health benefits including better cognitive skills among breast-fed compared with formula-fed infants. We conclude, based on evidence from other studies, that the benefits of breast-feeding probably outweigh any risk from PCB exposures via breast milk among the four New Bedford infants. In this case report, PCB analysis of breast milk and infant cord serum was a research tool. PCB analysis of milk is rarely done clinically, in part because it is difficult to use the results of such analyses to predict health risks. Substantial effort is needed to achieve a better understanding of the clinical and public health significance of PCB exposures, particularly among potentially susceptible groups such as infants and children. Such efforts are critical to improving the clinical and public health management of widespread and ongoing population exposures to PCBs.
Images
PMCID: PMC1533214  PMID: 9681980
10.  Prenatal exposure to polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) may influence birth weight among infants in a Swedish cohort with background exposure: a cross-sectional study 
Environmental Health  2013;12:44.
Background
Prenatal exposure to persistent organic pollutants, e.g. polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) has been suggested to negatively affect birth weight although epidemiological evidence is still inconclusive. We investigated if prenatal exposure to PCBs and PBDEs is related to birth weight in a Swedish population with background exposure.
Methods
Breast milk was sampled during the third week after delivery from first-time mothers in Uppsala county, Sweden 1996–2010 (POPUP cohort) (N = 413). Samples were analysed for di-ortho PCBs (CB-138, 153, 180) and tetra- to hexa- brominated PBDEs (BDE-47, 99, 100, 153). Simple and multiple linear regression models were used to investigate associations between lipid-adjusted, ln-transformed PCB and PBDE concentrations, and birth weight. Covariates included in the multivariate regression model were PCB and PBDE exposure, maternal age, pre-pregnancy BMI, weight gain during pregnancy, education, smoking, gender of the infant and gestational length. The effect of including fish consumption was also investigated.
Results
In the multivariate model, prenatal exposure to di-ortho PCBs was significantly associated with increased birth weight (β = 137; p = 0.02). The result did not change when gestational length was added to the model. An inverse association between PBDE(4) (sum of BDE-47, -99, -100 and −153) and birth weight was observed in the multivariate model including gestational length (β = −106; p = 0.04). Maternal pre-pregnancy BMI and weight gain during pregnancy were important confounders of the association between di-ortho PCBs and birth weight. The associations were not alleviated after adjustment for fish consumption, a major source of PCB and PBDE exposure. The observed associations were stronger for boys than for girls.
Conclusions
Our results indicate that prenatal exposure to di-ortho PCBs and PBDE(4) may influence birth weight in different directions, i.e. PCB exposure was associated with higher birth weight and PBDE exposure with lower birth weight. Maternal pre-pregnancy BMI and weight gain during pregnancy were important confounders that may hide positive association between di-ortho PCB exposure and birth weight if they are not included in the statistical model. We speculate that even small PCB- and PBDE-induced shifts in the distribution of birth weight may influence future public health in populations with background exposure.
doi:10.1186/1476-069X-12-44
PMCID: PMC3673870  PMID: 23724965
Birth weight; Breast milk; PBDE; PCB; BMI; Weight gain; Fish consumption
11.  Long-Term Exposure to Silica Dust and Risk of Total and Cause-Specific Mortality in Chinese Workers: A Cohort Study 
PLoS Medicine  2012;9(4):e1001206.
A retro-prospective cohort study by Weihong Chen and colleagues provides new estimates for the risk of total and cause-specific mortality due to long-term silica dust exposure among Chinese workers.
Background
Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations.
Methods and Findings
We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job–exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure–response relationships between CDE (measured in milligrams/cubic meter–years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023–1.029), respiratory diseases (1.069, 1.064–1.074), respiratory tuberculosis (1.065, 1.059–1.071), and cardiovascular disease (1.031, 1.025–1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01–1.11), ischemic heart disease (1.65, 1.35–1.99), and pneumoconiosis (11.01, 7.67–14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m3. After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives.
Conclusions
Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Walk along most sandy beaches and you will be walking on millions of grains of crystalline silica, one of the commonest minerals on earth and a major ingredient in glass and in ceramic glazes. Silica is also used in the manufacture of building materials, in foundry castings, and for sandblasting, and respirable (breathable) crystalline silica particles are produced during quarrying and mining. Unfortunately, silica dust is not innocuous. Several serious diseases are associated with exposure to this dust, including silicosis (a chronic lung disease characterized by scarring and destruction of lung tissue), lung cancer, and pulmonary tuberculosis (a serious lung infection). Moreover, exposure to silica dust increases the risk of death (mortality). Worryingly, recent reports indicate that in the US and Europe, about 1.7 and 3.0 million people, respectively, are occupationally exposed to silica dust, figures that are dwarfed by the more than 23 million workers who are exposed in China. Occupational silica exposure, therefore, represents an important global public health concern.
Why Was This Study Done?
Although the lung-related adverse health effects of exposure to silica dust have been extensively studied, silica-related health effects may not be limited to these diseases. For example, could silica dust particles increase the risk of cardiovascular disease (diseases that affect the heart and circulation)? Other environmental particulates, such as the products of internal combustion engines, are associated with an increased risk of cardiovascular disease, but no one knows if the same is true for silica dust particles. Moreover, although it is clear that high levels of exposure to silica dust are dangerous, little is known about the adverse health effects of lower exposure levels. In this cohort study, the researchers examined the effect of long-term exposure to silica dust on the risk of all cause and cause-specific mortality in a large group (cohort) of Chinese workers.
What Did the Researchers Do and Find?
The researchers estimated the cumulative silica dust exposure for 74,040 workers at 29 metal mines and pottery factories from 1960 to 2003 from individual work histories and more than four million measurements of workplace dust concentrations, and collected health and mortality data for all the workers. Death from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 deaths per 100,000 person-years), and there was a positive exposure–response relationship between silica dust exposure and death from all causes, respiratory diseases, respiratory tuberculosis, and cardiovascular disease. For example, the hazard ratio for all cause death was 1.026 for every increase in cumulative silica dust exposure of 1 mg/m3-year; a hazard ratio is the incidence of an event in an exposed group divided by its incidence in an unexposed group. Notably, there was significantly increased mortality from all causes, ischemic heart disease, and silicosis among workers exposed to respirable silica concentrations at or below 0.1 mg/m3, the workplace exposure limit for silica dust set by the US Occupational Safety and Health Administration. For example, the standardized mortality ratio (SMR) for silicosis among people exposed to low levels of silica dust was 11.01; an SMR is the ratio of observed deaths in a cohort to expected deaths calculated from recorded deaths in the general population. Finally, the researchers used their data to estimate that, in 2008, 4.2% of deaths among industrial workers in China (231,104 deaths) were attributable to silica dust exposure.
What Do These Findings Mean?
These findings indicate that long-term silica dust exposure is associated with substantially increased mortality among Chinese workers. They confirm that there is an exposure–response relationship between silica dust exposure and a heightened risk of death from respiratory diseases and lung cancer. That is, the risk of death from these diseases increases as exposure to silica dust increases. In addition, they show a significant relationship between silica dust exposure and death from cardiovascular diseases. Importantly, these findings suggest that even levels of silica dust that are considered safe increase the risk of death. The accuracy of these findings may be affected by the accuracy of the silica dust exposure estimates and/or by confounding (other factors shared by the people exposed to silica such as diet may have affected their risk of death). Nevertheless, these findings highlight the need to tighten regulations on workplace dust control in China and elsewhere.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001206.
The American Lung Association provides information on silicosis
The US Centers for Disease Control and Prevention provides information on silica in the workplace, including links to relevant US National Institute for Occupational Health and Safety publications, and information on silicosis and other pneumoconioses
The US Occupational Safety and Health Administration also has detailed information on occupational exposure to crystalline silica
What does silicosis mean to you is a video provided by the US Mine Safety and Health Administration that includes personal experiences of silicosis; Dont let silica dust you is a video produced by the Association of Occupational and Environmental Clinics that identifies ways to reduce silica dust exposure in the workplace
The MedlinePlus encyclopedia has a page on silicosis (in English and Spanish)
The International Labour Organization provides information on health surveillance for those exposed to respirable crystalline silica
The World Health Organization has published a report about the health effects of crystalline silica and quartz
doi:10.1371/journal.pmed.1001206
PMCID: PMC3328438  PMID: 22529751
12.  Serum Concentrations of Polychlorinated Biphenyls in Relation to in Vitro Fertilization Outcomes 
Environmental Health Perspectives  2011;119(7):1010-1016.
Background: Human exposure to polychlorinated biphenyls (PCBs) remains widespread. PCBs have been associated with adverse reproductive health outcomes including reduced fecundability and increased risk of pregnancy loss, although the human data remain largely inconclusive.
Objective: Our goal was to explore the relationship between serum PCB concentrations and early pregnancy loss among a large cohort of women undergoing in vitro fertilization (IVF) between 1994 and 2003.
Methods: Concentrations of 57 PCB congeners were measured in serum samples collected during 827 IVF/intracytoplasmic sperm injection cycles from 765 women. Joint statistical models that accommodate multiple outcomes and multiple cycles per woman were used to assess the relationship between serum PCB quartiles and implantation failure, chemical pregnancies (human chorionic gonadotropin level > 5.0 mIU/mL) that did not result in clinical pregnancy, or spontaneous abortion, while also adjusting for confounders.
Results: PCB-153 was the congener present in the highest concentration (median, 46.2 ng/g lipid). Increasing quartiles of PCB-153 and the sum of all measured PCB congeners (ΣPCBs) were associated with significantly elevated dose-dependent odds of failed implantation. Adjusted odds ratios (95% confidence interval) for highest versus lowest quartile were 2.0 (1.2–3.4) for PCB-153 and 1.7 (1.0–2.9) for ΣPCBs. There were suggestive trends for increased odds of implantation failure for PCB-118 and cytochrome P450–inducing congeners (p-values for trend = 0.06). No statistically significant associations between PCBs and chemical pregnancy or spontaneous abortion were found.
Conclusions: Serum PCB concentrations at levels similar to the U.S. general population were associated with failed implantation among women undergoing IVF. These findings may help explain previous reports of reduced fecundability among women exposed to PCBs.
doi:10.1289/ehp.1002922
PMCID: PMC3222973  PMID: 21345762
environment; epidemiology; female; organochlorine; reproduction
13.  Polychlorinated Biphenyls (PCBs) Enhance Metastatic Properties of Breast Cancer Cells by Activating Rho-Associated Kinase (ROCK) 
PLoS ONE  2010;5(6):e11272.
Background
Polychlorinated biphenyls (PCBs) are a family of structurally related chlorinated aromatic hydrocarbons. Numerous studies have documented a wide spectrum of biological effects of PCBs on human health, such as immunotoxicity, neurotoxocity, estrogenic or antiestrogenic activity, and carcinogensis. The role of PCBs as etiologic agents for breast cancer has been intensively explored in a variety of in vivo, animal and epidemiologic studies. A number of investigations indicated that higher levels of PCBs in mammary tissues or sera correlated to breast cancer risk, and PCBs might be implicated in advancing breast cancer progression.
Methodology/Principal Findings
In the current study, we for the first time report that PCBs greatly promote the ROCK activity and therefore increase cell motility for both non-metastatic and metastatic human breast cancer cells in vitro. In the in vivo study, PCBs significantly advance disease progression, leading to enhanced capability of metastatic breast cancer cells to metastasize to bone, lung and liver. Additionally, PCBs robustly induce the production of intracellular reactive oxygen species (ROS) in breast cancer cells; ROS mechanistically elevate ROCK activity.
Conclusions/Significance
PCBs enhance the metastatic propensity of breast cancer cells by activating the ROCK signaling, which is dependent on ROS induced by PCBs. Inhibition of ROCK may stand for a unique way to restrain metastases in breast cancer upon PCB exposure.
doi:10.1371/journal.pone.0011272
PMCID: PMC2890589  PMID: 20585605
14.  Investigating Intergenerational Differences in Human PCB Exposure due to Variable Emissions and Reproductive Behaviors 
Environmental Health Perspectives  2010;119(5):641-646.
Background
Reproductive behaviors—such as age of childbearing, parity, and breast-feeding prevalence—have changed over the same historical time period as emissions of polychlorinated biphenyls (PCB) and may produce intergenerational differences in human PCB exposure.
Objectives
Our goal in this study was to estimate prenatal, postnatal, and lifetime PCB exposures for women at different ages according to year of birth, and to evaluate the impact of reproductive characteristics on intergenerational differences in exposure.
Methods
We used the time-variant mechanistic model CoZMoMAN to calculate human bioaccumulation of PCBs, assuming both hypothetical constant and realistic time-variant emissions.
Results
Although exposure primarily depends on when an individual was born relative to the emission history of PCBs, reproductive behaviors can have a significant impact. Our model suggests that a mother’s reproductive history has a greater influence on the prenatal and postnatal exposures of her children than it does on her own cumulative lifetime exposure. In particular, a child’s birth order appears to have a strong influence on their prenatal exposure, whereas postnatal exposure is determined by the type of milk (formula or breast milk) fed to the infant.
Conclusions
Prenatal PCB exposure appears to be delayed relative to the time of PCB emissions, particularly among those born after the PCB production phaseout. Consequently, the health repercussions of environmental PCBs can be expected to persist for several decades, despite bans on their production for > 40 years.
doi:10.1289/ehp.1002415
PMCID: PMC3094414  PMID: 21156396
environmental fate; human exposure; reproductive characteristics; modeling organic contaminants; PCBs; time-variant emissions
15.  Mitigation of building-related polychlorinated biphenyls in indoor air of a school 
Environmental Health  2012;11:24.
Background
Sealants and other building materials sold in the U.S. from 1958 - 1971 were commonly manufactured with polychlorinated biphenyls (PCBs) at percent quantities by weight. Volatilization of PCBs from construction materials has been reported to produce PCB levels in indoor air that exceed health protective guideline values. The discovery of PCBs in indoor air of schools can produce numerous complications including disruption of normal operations and potential risks to health. Understanding the dynamics of building-related PCBs in indoor air is needed to identify effective strategies for managing potential exposures and risks. This paper reports on the efficacy of selected engineering controls implemented to mitigate concentrations of PCBs in indoor air.
Methods
Three interventions (ventilation, contact encapsulation, and physical barriers) were evaluated in an elementary school with PCB-containing caulk and elevated PCB concentrations in indoor air. Fluorescent light ballasts did not contain PCBs. Following implementation of the final intervention, measurements obtained over 14 months were used to assess the efficacy of the mitigation methods over time as well as temporal variability of PCBs in indoor air.
Results
Controlling for air exchange rates and temperature, the interventions produced statistically significant (p < 0.05) reductions in concentrations of PCBs in indoor air of the school. The mitigation measures remained effective over the course of the entire follow-up period. After all interventions were implemented, PCB levels in indoor air were associated with indoor temperature. In a "broken-stick" regression model with a node at 20°C, temperature explained 79% of the variability of indoor PCB concentrations over time (p < 0.001).
Conclusions
Increasing outdoor air ventilation, encapsulating caulk, and constructing a physical barrier over the encapsulated material were shown to be effective at reducing exposure concentrations of PCBs in indoor air of a school and also preventing direct contact with PCB caulk. In-place management methods such as these avoid the disruption and higher costs of demolition, disposal and reconstruction required when PCB-containing building materials are removed from a school. Because of the influence of temperature on indoor air PCB levels, risk assessment results based on short-term measurements, e.g., a single day or season, may be erroneous and could lead to sub-optimal allocation of resources.
doi:10.1186/1476-069X-11-24
PMCID: PMC3353159  PMID: 22490055
Remediation; Abatement; Flux; Risk management
16.  Environmental organochlorine exposure as a potential etiologic factor in breast cancer. 
Environmental Health Perspectives  1995;103(Suppl 7):141-145.
Known risk factors for breast cancer do not account for a significant proportion of the overall incidence. Reproductive factors and endogenous hormones are thought to be responsible for a large component of risk. An environmental contribution has been sought in the past to explain the international trends in breast cancer rates and changes in risk among migrating populations. Recently, environmental research has turned to investigation of exogenous chemical exposures, including environmental contamination, as potential risk factors that may arise from the hormonal activity or from the carcinogenicity of many of these chemicals. Several reports since 1991 suggest that organochlorines may be a risk factor for breast cancer. The data are strongest for DDT. For PCBs, the results to date have been equivocal if not entirely negative. However, different groups of polychlorinated biphenyl (PCB) congeners are known to provoke biological responses that are structure specific. A wide divergence of estrogenic response, cytochrome P450 activity, and biological half-life exists within these groups of PCB congeners. Therefore, understanding breast cancer risk from PCB exposure requires attention to congener structures in complex mixtures and to temporal changes in exposure. Investigation of environmental contributions to breast cancer risk offers the potential for understanding more about the etiology of this complex disease and may also provide opportunities for prevention of the most common cancer among women in the United States.
PMCID: PMC1518872  PMID: 8593861
17.  Environmental Exposure to Polychlorinated Biphenyls and p,p´-DDE and Sperm Sex-Chromosome Disomy 
Environmental Health Perspectives  2011;120(4):535-540.
Background: Chromosomal abnormalities contribute substantially to reproductive problems, but the role of environmental risk factors has received little attention.
Objectives: We evaluated the association of polychlorinated biphenyl (PCB) and dichlorodiphenyldichloroethylene (p,p´-DDE) exposures with sperm sex-chromosome disomy.
Methods: We conducted a cross-sectional study of 192 men from subfertile couples. We used multiprobe fluorescence in situ hybridization (FISH) for chromosomes X, Y, and 18 to determine XX, YY, XY, and total sex-chromosome disomy in sperm nuclei. Serum was analyzed for concentrations of 57 PCB congeners and p,p´-DDE. Poisson regression models were used to calculate incidence rate ratios (IRRs) for disomy by exposure quartiles, controlling for demographic characteristics and semen parameters.
Results: The median percent disomy was 0.3 for XX and YY, 0.9 for XY, and 1.6 for total sex-chromosome disomy. We observed a significant trend of increasing IRRs for increasing quartiles of p,p´-DDE in XX, XY, and total sex-chromosome disomy, and a significant trend of increasing IRRs for increasing quartiles of PCBs for XY and total sex-chromosome disomy; however, there was a significant inverse association for XX disomy.
Conclusions: Our findings suggest that exposure to p,p´-DDE may be associated with increased rates of XX, XY, and total sex-chromosome disomy, whereas exposure to PCBs may be associated with increased rates of YY, XY, and total sex-chromosome disomy. In addition, we observed an inverse association between increased exposure to PCBs and XX disomy. Further work is needed to confirm these findings.
doi:10.1289/ehp.1104017
PMCID: PMC3339457  PMID: 22189045
aneuploidy; dichlorodiphenyltrichloroethane (DDT); dichlorodiphenyldichloroethylene (DDE); disomy; endocrine disruptors; in situ hybridization; fluorescence; pesticides; polychlorinated biphenyls (PCBs); reproduction; sperm
18.  Predictors of Serum Dioxins and PCBs among Peripubertal Russian Boys 
Environmental Health Perspectives  2009;117(10):1593-1599.
Background
Although sources and routes of exposure to dioxins and polychlorinated biphenyls (PCBs) have been studied, information regarding exposure among children is limited. Breast-feeding and diet are two important contributors to early life exposure. To further understand other significant contributors to childhood exposure, we studied a cohort of children from a city with high environmental dioxin levels.
Objectives
We investigated predictors of serum concentrations of polychlorinated dibenzo-p-dioxins (PCDDs)/polychlorinated dibenzofurans (PCDFs)/co-planar PCBs (C-PCBs), toxic equivalents (TEQs), and PCBs among 8- to 9-year-old boys in Chapaevsk, Russia.
Methods
We used general linear regression models to explore associations of log10-transformed serum concentrations of PCDDs/PCDFs/C-PCBs, TEQs, and PCBs at study entry with anthropometric, demographic, geographic, and dietary factors in 482 boys in Chapaevsk, Russia.
Results
The median (25th, 75th percentile) concentration for total 2005 TEQs was 21.1 pg/g lipid (14.4, 33.2). Boys who were older, consumed local foods, were breast-fed longer, and whose mothers were employed at the Khimprom chemical plant (where chlorinated chemicals were produced) or gardened locally had significantly higher serum dioxins and PCBs, whereas boys with higher body mass index or more educated parents had significantly lower serum dioxins and PCBs. Boys who lived < 2 km from Khimprom had higher total TEQs (picograms per gram lipid) [adjusted mean = 30.6; 95% confidence interval (CI), 26.8–35.0] than boys who lived > 5 km away (adjusted mean = 18.8; 95% CI, 17.2–20.6).
Conclusions
Our findings suggest that there are specific local sources of dioxin and PCB exposure among children in Chapaevsk including maternal gardening, consumption of locally grown food, and residential proximity to the Khimprom plant.
doi:10.1289/ehp.0800223
PMCID: PMC2790515  PMID: 20019911
children; diet; environment; epidemiology; polychlorinated biphenyls; polychlorinated dibenzodioxins; polychlorinated dibenzofurans
19.  Assessment of exposure to PCB 153 from breast feeding and normal food intake in individual children using a system approach model 
Chemosphere  2011;85(11):1687-1693.
Investigators have typically relied on a single or few discrete time points as measures of polychlorinated biphenyl (PCB) body burden, however health effects are more likely to be the result of integrative exposure in time, optionally expressed as an area under the time curve (AUC) of PCB serum concentration. Using data from a subgroup of 93 infants from a birth cohort in eastern Slovakia—a region highly polluted by PCBs—we fit a system type model, customized to our longitudinal measures of serum PCB concentrations in cord, 6, 16, and, 45 month blood specimens. The most abundant congener, PCB 153, was chosen for modeling purposes. In addition to currently used methods of exposure assessment, our approach estimates a concentration time profile for each subject, taking into account mean residence time of PCB 153 molecules in the body, duration of breast feeding, hypothetical PCB 153 concentration in steady-state without breast feeding and alternately without normal food intake. Hypothetical PCB 153 concentration in steady-state without normal food intake correlates with AUC (r=0.84, p<0.001) as well as with duration of breast feeding (r=0.64, p<0.001). It makes possible to determine each subject’s exposure profile expressed as AUC of PCBs serum concentration with a minimum model parameters. PCB body burden in most infants was strongly associated with duration of breast feeding in most, but not all children, was apparent from model output.
doi:10.1016/j.chemosphere.2011.09.013
PMCID: PMC3228605  PMID: 22051344
Polychlorinated biphenyls; Breast feeding; Toxicokinetics; Modeling; Mean residence time; Children
20.  Uterine Leiomyomata in a Cohort of Great Lakes Sport Fish Consumers 
Environmental research  2011;111(4):565-572.
Diet and endocrine disrupting persistent organic pollutants (POPs) have been associated with gynecologic conditions including uterine leiomyomata (UL), endometriosis, and ovarian cysts. Great Lakes sport fish consumption is a source of exposure to POPs such as p,p’-diphenyldichloroethene (DDE) and polychlorinated biphenyls (PCBs). This study was designed to examine retrospectively the effects Great Lakes sport fish consumption on the incidence of UL and to examine the effects of DDE and PCB serum levels on prevalent UL in women participating in the Great Lakes Fish Consumption Study. We hypothesized that associations of exposures with UL would be modified by breastfeeding status. Years of sport fish consumption, demographic, health, and reproductive data were assessed by survey. In a subgroup, serum was collected and tested for DDE and PCB levels. Effects of years of Great Lakes sport fish and sport fish consumption were modeled using time-dependent Cox proportional hazards regression and effects of POP exposures on UL were modeled using multiple logistic regression. Years of sport fish consumption were associated with UL, with an incidence rate ratio of 1.2 (95% CI 1.0-1.3) for each 10-year increment of fish consumption. Summary measures of POP exposures in the overall group were not associated with UL. In the subgroup of women who never breastfed and in whom PCB measurements were available, however, UL was significantly associated with PCBs and groupings of estrogenic, antiestrogenic, and dioxin-like PCBs. These findings support the possibility that PCB exposures from fish consumption may increase the risk of UL and highlight the importance of additional studies exploring biologic pathways by which they could be acting.
doi:10.1016/j.envres.2011.01.006
PMCID: PMC3111144  PMID: 21310402
DDE; fibroids; Great Lakes sport fish; leiomyomata; PCBs
21.  Birth Weight and Prenatal Exposure to Polychlorinated Biphenyls (PCBs) and Dichlorodiphenyldichloroethylene (DDE): A Meta-analysis within 12 European Birth Cohorts 
Environmental Health Perspectives  2011;120(2):162-170.
Objectives: Exposure to high concentrations of persistent organochlorines may cause fetal toxicity, but the evidence at low exposure levels is limited. Large studies with substantial exposure contrasts and appropriate exposure assessment are warranted. Within the framework of the EU (European Union) ENRIECO (ENvironmental Health RIsks in European Birth Cohorts) and EU OBELIX (OBesogenic Endocrine disrupting chemicals: LInking prenatal eXposure to the development of obesity later in life) projects, we examined the hypothesis that the combination of polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethylene (DDE) adversely affects birth weight.
Methods: We used maternal and cord blood and breast milk samples of 7,990 women enrolled in 15 study populations from 12 European birth cohorts from 1990 through 2008. Using identical variable definitions, we performed for each cohort linear regression of birth weight on estimates of cord serum concentration of PCB-153 and p,p´-DDE adjusted for gestational age and a priori selected covariates. We obtained summary estimates by meta-analysis and performed analyses of interactions.
Results: The median concentration of cord serum PCB-153 was 140 ng/L (range of cohort medians 20–484 ng/L) and that of p,p´-DDE was 528 ng/L (range of cohort medians 50–1,208 ng/L). Birth weight decreased with increasing cord serum concentration of PCB-153 after adjustment for potential confounders in 12 of 15 study populations. The meta-analysis including all cohorts indicated a birth weight decline of 150 g [95% confidence interval (CI): –250, –50 g] per 1-µg/L increase in PCB-153, an exposure contrast that is close to the range of exposures across the cohorts. A 1-µg/L increase in p,p´-DDE was associated with a 7-g decrease in birth weight (95% CI: –18, 4 g).
Conclusions: The findings suggest that low-level exposure to PCB (or correlated exposures) impairs fetal growth, but that exposure to p,p´-DDE does not. The study adds to mounting evidence that low-level exposure to PCBs is inversely associated with fetal growth.
doi:10.1289/ehp.1103767
PMCID: PMC3279442  PMID: 21997443
birth cohort studies; DDE; gestational age; meta-analysis; PCBs; reproductive effects
22.  Health status and PCBs in blood of workers exposed to PCBs and of their children. 
A follow-up study of capacitor manufacturing workers exposed to polychlorinated biphenyls (PCBs) and their children was conducted since 1973. PCB levels in whole blood of workers as well as in breast milk of the exposed lactating mothers were approximately 10 to 100 times those of nonexposed Japanese. Blood PCB levels had a statistically significant correlation with the duration of PCB handling and breast milk PCB levels. The rate of decline of blood PCB levels, as well as the changes of the gas chromatograph of blood PCB over 7 years was found to vary with the kind of PCB handled. The levels of blood PCB tended to be higher in the children fed PCB-contaminated breast milk for a long period. The great majority of workers handling PCBs had dermatologic complaints. Discontinuance of contact with PCB led to gradual improvement of these lesions. Abnormal results in the blood chemistry of the workers were rare, while serum triglyceride concentration was significantly correlated with blood PCB levels in 1974. In the questionnaire study, the number of complaints in children born from mothers who had handled PCBs, especially those fed breast milk for a long period, was conspicuously higher than that in control groups. Several children were found to have the same medical findings as in yusho; however, they have not been diagnosed as PCB-poisoning, because these findings were neither so serious nor related to the blood PCB levels.
PMCID: PMC1568101  PMID: 3921370
23.  Polychlorinated biphenyls, cytochrome P450 1A1 (CYP1A1) polymorphisms, and breast cancer risk among African American women and white women in North Carolina: a population-based case-control study 
Breast Cancer Research  2004;7(1):R12-R18.
Introduction
Epidemiologic studies have not shown a strong relationship between blood levels of polychlorinated biphenyls (PCBs) and breast cancer risk. However, two recent studies showed a stronger association among postmenopausal white women with the inducible M2 polymorphism in the cytochrome P450 1A1 (CYP1A1) gene.
Methods
In a population-based case-control study, we evaluated breast cancer risk in relation to PCBs and the CYP1A1 polymorphisms M1 (also known as CYP1A1*2A), M2 (CYP1A1*2C), M3 (CYP1A1*3), and M4 (CYP1A1*4). The study population consisted of 612 patients (242 African American, 370 white) and 599 controls (242 African American, 357 white).
Results
There was no evidence of strong joint effects between CYP1A1 M1-containing genotypes and total PCBs in African American or white women. Statistically significant multiplicative interactions were observed between CYP1A1 M2-containing genotypes and elevated plasma total PCBs among white women (P value for likelihood ratio test = 0.02). Multiplicative interactions were also observed between CYP1A1 M3-containing genotypes and elevated total PCBs among African American women (P value for likelihood ratio test = 0.10).
Conclusions
Our results confirm previous reports that CYP1A1 M2-containing genotypes modify the association between PCB exposure and risk of breast cancer. We present additional evidence suggesting that CYP1A1 M3-containing genotypes modify the effects of PCB exposure among African American women. Additional studies are warranted, and meta-analyses combining results across studies will be needed to generate more precise estimates of the joint effects of PCBs and CYP1A1 genotypes.
doi:10.1186/bcr941
PMCID: PMC1064095  PMID: 15642161
breast cancer; CYP1A1; polychlorinated biphenyls
24.  Occupation and occupational exposure to endocrine disrupting chemicals in male breast cancer: a case-control study in Europe 
Objectives
Male breast cancer is a rare disease of largely unknown etiology. Besides genetic or hormone-related risk factors, a large number of environmental chemicals are suspected to play a role in breast cancer. The identification of occupations or occupational exposures associated with an increased incidence of breast cancer in men may help to identify mammary carcinogens in the environment.
Methods
Occupational risk factors of male breast cancer were investigated in a multi-centre case-control study conducted in 8 European countries, including 104 cases and 1901 controls. Lifetime work history was obtained during in-person interviews. Occupational exposures to endocrine disrupting chemicals (alkylphenolic compounds, phthalates, PCBs and dioxins) were assessed on a case-by-case basis from expert judgment.
Results
Male breast cancer incidence was more particularly increased in motor vehicle mechanics (OR=2.1, CI 1.0–4.4) with a dose-effect relationship with duration employment. It was also increased in paper makers and painters, and in workers in forestry and logging, health and social work, and manufacture of furniture. The odds ratio for exposure to alkylphenolic compounds above median was 3.8 (CI 1.5–9.5). This association persisted after adjustment for occupational exposures to other environmental estrogens.
Conclusion
These findings suggest that some environmental chemicals are possible mammary carcinogens. Gasoline, organic petroleum solvents or PAH can be suspected from the consistent elevated risk of male breast cancer observed in motor vehicle mechanics. Endocrine disruptors such as alkylphenolic compounds may play a role in breast cancer.
doi:10.1136/oem.2009.052175
PMCID: PMC3151527  PMID: 20798010
Case-Control Studies; Occupations; Occupational Exposures; Breast Neoplasms,Male; Endocrine Disruptors
25.  Allergy and Sensitization during Childhood Associated with Prenatal and Lactational Exposure to Marine Pollutants 
Environmental Health Perspectives  2010;118(10):1429-1433.
Background
Breast-feeding may affect the risk of developing allergy during childhood and may also cause exposure to immunotoxicants, such as polychlorinated biphenyls (PCBs), which are of concern as marine pollutants in the Faroe Islands and the Arctic region.
Objectives
The objective was to assess whether sensitization and development of allergic disease is associated with duration of breast-feeding and prenatal or postnatal exposures to PCBs and methylmercury.
Methods
A cohort of 656 singleton births was formed in the Faroe Islands during 1999–2001. Duration of breast-feeding and history of asthma and atopic dermatitis were recorded at clinical examinations at 5 and 7 years of age. PCB and mercury concentrations were determined in blood samples obtained at parturition and at follow-up. Serum from 464 children (71%) at 7 years of age was analyzed for total immunoglobulin E (IgE) and grass-specific IgE.
Results
The total IgE concentration in serum at 7 years of age was positively associated both with the concomitant serum PCB concentration and with the duration of breast-feeding. However, the effect only of the latter was substantially attenuated in a multivariate analysis. A raised grass-specific IgE concentration compatible with sensitization was positively associated with the duration of breast-feeding and inversely associated with prenatal methylmercury exposure. However, a history of asthma or atopic dermatitis was not associated with the duration of breast-feeding, although children with atopic dermatitis had lower prenatal PCB exposures than did nonallergic children.
Conclusions
These findings suggest that developmental exposure to immunotoxicants may both increase and decrease the risk of allergic disease and that associations between breast-feeding and subsequent allergic disease in children may, at least in part, reflect lactational exposure to immunotoxic food contaminants.
doi:10.1289/ehp.1002289
PMCID: PMC2957924  PMID: 20562055
allergy; breast-feeding; developmental toxicity; environmental exposure; immunotoxicity; methylmercury; polychlorinated biphenyls

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