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1.  Associations of maternal prenatal dietary intake of n-3 and n-6 fatty acids with maternal and umbilical cord blood levels☆ 
Maternal n-3 and n-6 polyunsaturated fatty acid (PUFA) status may influence birth outcomes and child health. We assessed second trimester maternal diet with food frequency questionnaires (FFQs) (n = 1666), mid-pregnancy maternal erythrocyte PUFA concentrations (n = 1550), and umbilical cord plasma PUFA concentrations (n = 449). Mean (SD) maternal intake of total n-3 PUFA was 1.17 g/d (0.43), docosahexaenoic and eicosapentaenoic acids (DHA+EPA) 0.16 g/d (0.17), and total n-6 PUFA 12.25 g/d (3.25). Mean maternal erythrocyte and cord plasma PUFA concentrations were 7.0% and 5.2% (total n-3), 5.0% and 4.6% (DHA+EPA), and 27.9% and 31.4% (total n-6). Mid-pregnancy diet–blood and blood–blood correlations were strongest for DHA+EPA (r = 0.38 for diet with maternal blood, r = 0.34 for diet with cord blood, r = 0.36 for maternal blood with cord blood), and less strong for n-6 PUFA. The FFQ is a reliable measure of elongated PUFA intake, although inter-individual variation is present
PMCID: PMC3939614  PMID: 19380219
Pregnancy; Diet; n-3 fatty acids; n-6 fatty acids
2.  Ambient particulate air pollution and cardiac arrhythmia in a panel of older adults in Steubenville, Ohio 
Ambient particulate air pollution has been associated with increased risk of cardiovascular morbidity and mortality. Pathways by which particles may act involve autonomic nervous system dysfunction or inflammation, which can affect cardiac rate and rhythm. The importance of these pathways may vary by particle component or source. In an eastern US location with significant regional pollution, the authors examined the association of air pollution and odds of cardiac arrhythmia in older adults.
Thirty two non‐smoking older adults were evaluated on a weekly basis for 24 weeks during the summer and autumn of 2000 with a standardised 30 minute protocol that included continuous electrocardiogram measurements. A central ambient monitoring station provided daily concentrations of fine particles (PM2.5, sulfate, elemental carbon) and gases. Sulfate was used as a marker of regional pollution. The authors used logistic mixed effects regression to examine the odds of having any supraventricular ectopy (SVE) or ventricular ectopy (VE) in association with increases in air pollution for moving average pollutant concentrations up to 10 days before the health assessment.
Participant specific mean counts of arrhythmia over the protocol varied between 0.1–363 for SVE and 0–350 for VE. The authors observed odds ratios for having SVE over the length of the protocol of 1.42 (95% CI 0.99 to 2.04), 1.70 (95% CI 1.12 to 2.57), and 1.78 (95% CI 0.95 to 3.35) for 10.0 μg/m3, 4.2 μg/m3, and 14.9 ppb increases in five day moving average PM2.5, sulfate, and ozone concentrations respectively. The other pollutants, including elemental carbon, showed no effect on arrhythmia. Participants reporting cardiovascular conditions (for example, previous myocardial infarction or hypertension) were the most susceptible to pollution induced SVE. The authors found no association of pollution with VE.
Increased levels of ambient sulfate and ozone may increase the risk of supraventricular arrhythmia in the elderly.
PMCID: PMC2078044  PMID: 16757505
air pollution; PM2.5; epidemiology; cardiovascular disease; arrhythmia
3.  Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility 
Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction—processes in which cell adhesion molecules and inflammatory markers play important roles.
To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes.
Daily average ambient levels of air pollution (fine particles (PM2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM‐1, VCAM‐1 and vWF. Linear regressions were fit to plasma levels of ICAM‐1, VCAM‐1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors.
Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM2.5, BC and VCAM‐1 were particularly strong.
These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution‐associated cardiovascular events among those with diabetes.
PMCID: PMC2078522  PMID: 17182639
4.  Mouse allergen exposure, wheeze and atopy in the first seven years of life 
Allergy  2008;63(11):1512-1518.
Little is known about mouse allergen exposure in home environments and the development of wheezing, asthma and atopy in childhood.
To examine the relation between mouse allergen exposure and wheezing, atopy, and asthma in the first 7 years of life.
Prospective study of 498 children with parental history of allergy or asthma followed from birth to age 7 years, with longitudinal questionnaire ascertainment of reported mouse exposure and dust sample mouse urinary protein allergen levels measured at age 2–3 months.
Parental report of mouse exposure in the first year of life was associated with increased risk of transient wheeze and wheezing in early life. Current report of mouse exposure was also significantly associated with current wheeze throughout the first 7 years of life in the longitudinal analysis (P = 0.03 for overall relation of current mouse to current wheeze). However, early life mouse exposure did not predict asthma, eczema or allergic rhinitis at age 7 years. Exposure to detectable levels of mouse urinary protein in house dust samples collected at age 2–3 months was associated with a twofold increase in the odds of atopy (sensitization to >=1 allergen) at school age (95% confidence interval for odds ratio = 1.1–3.7; P = 0.03 in a multivariate analysis.
Among children with parental history of asthma or allergies, current mouse exposure is associated with increased risk of wheeze during the first 7 years of life. Early mouse exposure was associated with early wheeze and atopy later in life.
PMCID: PMC2574689  PMID: 18616677
childhood asthma; indoor allergens; mouse allergen
5.  Fetal Cord Blood: Aspects of Heightened Immune Responses 
Journal of clinical immunology  2005;25(4):329-337.
Neonatal immune responses have been associated with the development of atopy in childhood. We assessed in cord blood mononuclear cells (CBMC) whether increased allergen/mitogen-induced lymphoproliferation (LP) is associated with pro-allergic Th2 cytokine IL-13 or Th1 cytokine IFN-γ secretion. We determined whether LP to one allergen is related to heightened lymphocyte function to other allergens/mitogen. CBMC from 135 neonates were stimulated with house dust mite (Derf1), cockroach, ovalbumin, or mitogen. LP to one allergen was associated with significantly increased LP to other allergens/mitogen. Increased Derf1-LP was associated with increased Derf1-induced IL-13 secretion (r = 0.21, p = 0.01). After adjusting for neonatal gender, race, and maternal smoking, Derf1-LP remained associated with Derf1-IL-13 (OR 3.08, 95% CI 1.56–6.10). Increased mitogen-induced proliferation was associated with increased mitogen-induced IL-13 secretion (r = 0.37, p < 0.001). For some individuals, a predisposition to a heightened immune response is already evident at birth. Whether this phenotype results in atopy in childhood warrants further investigation.
PMCID: PMC1488727  PMID: 16133989
Allergens; cord blood; immunology; lymphocytes; neonatal
6.  Predictors of indoor exposure to mouse allergen in urban and suburban homes in Boston 
Allergy  2005;60(5):697-701.
Mouse allergen exposure is prevalent among urban children with asthma. Little is known about mouse allergen exposure in children at risk for the development of allergic diseases.
Aims of the study
To assess indoor mouse allergen exposure in early life among children with parental history of asthma or allergies.
Prospective birth cohort study of 498 children with a history of allergy or asthma in at least one parent living in metropolitan Boston.
Of the 498 participating children, 357 (71.7%) resided outside the city of Boston and 439 (90.7%) lived in households with incomes >$30 000. Mouse allergen was detected in 42% of the homes of study participants. In a multivariate analysis adjusting for sex, income, and endotoxin, black race [odds ratio (OR) = 3.0; 95% confidence interval (CI) = 1.3–6.6, P = 0.009], signs of mice in the home at age 2–3 months (OR = 3.0; 95% CI = 1.6–5.6, P = 0.0006), and kitchen cockroach allergen levels ≥0.05 to <2 U/g (OR = 1.8; 95% CI = 1.1–3.2, P = 0.02) were associated with detectable mouse allergen in the kitchen. In this model, living in a single detached house was inversely associated with detectable kitchen mouse allergen levels (OR = 0.4; 95% CI = 0.2–0.6, P = 0.0001).
Infants with a parental history of asthma or allergies are commonly exposed to mouse allergen in their homes. Among infants at high risk for atopy, predictors of increased mouse allergen levels included black race, reported mice exposure, and moderate levels of cockroach allergen.
PMCID: PMC1283113  PMID: 15813819
mouse allergen; indoor allergens; childhood asthma; environment; MUP, mouse urinary protein; NPV, negative predictive value; OR, odds ratio; PPV, positive predictive value
7.  Predictors of airborne endotoxin in the home. 
Environmental Health Perspectives  2001;109(8):859-864.
We identified home characteristics associated with the level of airborne endotoxin in 111 Boston-area homes enrolled in a cohort study of home exposures and childhood asthma, and we developed a predictive model to estimate airborne endotoxin. We measured endotoxin in family-room air and in dust from the baby's bed, family room, bedroom, and kitchen floor. Level of airborne endotoxin was weakly correlated (r < 0.3) with level of endotoxin in each of the four types of dust samples and was significantly correlated with endotoxin in family-room dust (p < 0.05). Endotoxin in family-room dust accounted for < 6% of the variability of airborne endotoxin. In a multivariate model, certain home characteristics were positively (p < 0.05) associated with airborne endotoxin. These included current presence of dog (difference in level, dog vs. no dog = 72%, partial R(2 )= 12.8%), past presence of dog (partial R(2) = 5.5%), and endotoxin level in family-room dust (partial R(2) = 5.3%). Use of a dehumidifier (partial R(2) = 6.4%) was negatively associated (p = 0.02; difference = -31%) with airborne endotoxin. Other home characteristics were identified as important determinants of increased airborne endotoxin in this model, but individual coefficients were not statistically significant (alpha = 0.05): total amount of fine dust collected in the home (partial R(2 )= 3.8%), concrete floor in family room (3.7%), water damage (3.6%), and use of cool-mist humidifier in past year (2.7%). This multivariate model explained 42% of the variability of airborne endotoxin levels, a substantial improvement over that with dust endotoxin alone. Airborne endotoxin in Boston-area homes appears to be determined by the presence of dogs, moisture sources, and increased amounts of settled dust.
PMCID: PMC1240416  PMID: 11564624
8.  Acute exposure to environmental tobacco smoke and heart rate variability. 
Environmental Health Perspectives  2001;109(7):711-716.
Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers. We conducted ambulatory electrocardiographic (ECG) monitoring for 8-hr periods while participants alternated 2 hr in nonsmoking and smoking areas. Nicotine and respirable suspended particle concentrations and participants' blood oxygen saturation were also monitored. We calculated time and frequency domain measures of HRV for periods in and out of the smoking area, and we evaluated associations with ETS using comparative statistics and regression modeling. ETS exposure was negatively associated with all measures of HRV. During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ETS exposures were not associated with mean heart rate or blood oxygen saturation. Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.
PMCID: PMC1240375  PMID: 11485870
9.  Longitudinal study of dust and airborne endotoxin in the home. 
Environmental Health Perspectives  2000;108(11):1023-1028.
To characterize the seasonal variability of endotoxin levels, we measured endotoxin in dust from the bed, bedroom floor, and kitchen floor in 20 homes, and in air from the bedroom in 15 of the homes. All homes were located in the greater Boston, Massachusetts, area and were sampled each month from April 1995 to June 1996. Outdoor air was collected at two locations. We found greater within-home than between-home variance for bedroom floor, kitchen floor, and airborne endotoxin. However, the reverse was true for bed dust endotoxin. Thus, studies using single measurements of dust endotoxin are most likely to reliably distinguish between homes if bed dust is sampled. Dust endotoxin levels were not significantly associated with airborne endotoxin. Airborne endotoxin was significantly (p = 0. 04) and positively associated with absolute humidity in a mixed-effect model adjusting for a random home effect and fixed effect of sampling month and home characteristics. This finding implies that indoor humidity may be an important factor controlling endotoxin exposure. We found a significant (p < 0.05) seasonal effect in kitchen floor dust (spring > fall) and bedroom airborne endotoxin (spring > winter), but not in the other indoor samples. We found significant seasonal pattern in outdoor airborne endotoxin (summer > winter).
PMCID: PMC1240157  PMID: 11102291
10.  Environmental tobacco smoke, indoor allergens, and childhood asthma. 
Environmental Health Perspectives  2000;108(Suppl 4):643-651.
Both environmental tobacco smoke and indoor allergens can exacerbate already established childhood albeit primarily through quite disparate mechanisms. In infancy and childhood, environmental tobacco smoke (ETS) exposure is associated with measures of decreased flow in the airways, bronchial hyperresponsiveness, and increased respiratory infections, but the relationship between ETS and allergy is poorly understood. Indoor allergens from dust mite, cockroach, and cat can be associated with asthma exacerbation in children sensitized to the specific allergens. The precise role of either ETS or indoor allergens in the development of asthma is less well understood. The strong and consistent association between ETS and asthma development in young children may relate to both prenatal and postnatal influences on airway caliber or bronchial responsiveness. Dust mite allergen levels predict asthma in children sensitized to dust mite. The tendency to develop specific IgE antibodies to allergens (sensitization) is associated with and may be preceded by the development of a T-helper (Th)2 profile of cytokine release. The importance of either ETS or indoor allergens in the differentiation of T cells into a Th2-type profile of cytokine release or in the localization of immediate-type allergic responses to the lung is unknown. This article evaluates the strength of the evidence that ETS or indoor allergens influence asthma exacerbation and asthma development in children. We also selectively review data for the effectiveness of allergen reduction in reducing asthma symptoms and present a potential research agenda regarding these two broad areas of environmental exposure and their relationship to childhood asthma.
PMCID: PMC1637671  PMID: 10931782
11.  Socioeconomic predictors of high allergen levels in homes in the greater Boston area. 
Environmental Health Perspectives  2000;108(4):301-307.
In the United States, childhood asthma morbidity and prevalence rates are the highest in less affluent urban minority communities. More than 80% of childhood asthmatics are allergic to one or more inhalant allergens. We evaluated whether socioeconomic status was associated with a differential in the levels and types of indoor home allergens. Dust samples for an ELISA allergen assay were collected from the homes of 499 families as part of a metropolitan Boston, Massachusetts, longitudinal birth cohort study of home allergens and asthma in children with a parental history of asthma or allergy. The proportion of homes with maximum home allergen levels in the highest category was 42% for dust mite allergen (> or = 10 microg/g Der p 1 or Der f 1), 13% for cockroach allergen (> or = 2 U/g Bla g 1 or Bla g 2), 26% for cat allergen (> or = 8 microg/g Fel d 1), and 20% for dog allergen (> or = 10 microg/g Can f 1). Homes in the high-poverty area (> 20% of the population below the poverty level) were more likely to have high cockroach allergen levels than homes in the low-poverty area [51 vs. 3%; OR, 33; 95% confidence interval (CI), 12-90], but less likely to have high levels of dust mite allergen (16 vs. 53%; OR, 0.2; CI, 0.1-0.4). Lower family income, less maternal education, and race/ethnicity (black or Hispanic vs. white) were also associated with a lower risk of high dust mite levels and a greater risk of high cockroach allergen levels. Within a single U.S. metropolitan area we found marked between-community differences in the types of allergens present in the home, but not necessarily in the overall burden of allergen exposure.
PMCID: PMC1638021  PMID: 10753087
12.  Cockroach allergy and asthma in a 30-year-old man. 
Environmental Health Perspectives  1999;107(3):243-247.
A growing body of evidence has implicated allergens derived from cockroaches as an important environmental factor that may aggravate asthma in sensitized persons. We present the case of a 30-year-old man with asthma and a cockroach allergy. Allergy skin testing confirmed hypersensitivity to cockroach extract, and a home visit revealed visual evidence of infestation and the presence of Bla g 1 German cockroach allergen in vacuumed dust. As is typical of patients with a cockroach allergy and asthma, multiple factors in addition to cockroach allergen appeared to aggravate the patient's asthma. A multimodality therapeutic regimen, which included medications as well as cleaning of the home, integrated pest management, and professional application of chemical controls, resulted in substantial clinical improvement. The pathophysiology, epidemiology, and clinical features of cockroach-allergic asthma are reviewed, and an approach to diagnosis and management is suggested.
PMCID: PMC1566372  PMID: 10064555
13.  Mortality and ambient fine particles in southwest Mexico City, 1993-1995. 
Environmental Health Perspectives  1998;106(12):849-855.
++Epidemiologic studies have focused attention on the health effects of fine particulate air pollutants <2.5 microm in diameter (PM2.5). To further characterize the potential effects of fine particles, we investigated the relationship of air pollution to mortality in Mexico City during 1993-1995. The concentration of PM2.5 was measured on a 24-hr integrated basis; concentrations of NO2 and ozone were measured hourly and reduced to 24-hr means. Daily mortality was determined from death registration records, and Poisson regression was used to model daily death counts as a function of air pollutant levels on the same and previous days, while controlling for temperature and periodic cycles. Without taking other air pollutants into account, a 10 microg/m3 increase in the level of PM2.5 was associated with a 1.4% increase in total mortality, both on the current day and 4 days after exposure [95% confidence interval (CI), 0.2-2.5]. An equivalent increase in PM2.5 was also associated with somewhat larger excesses of deaths among people over 65 years of age and from cardiovascular and respiratory causes, which occurred after a lag of 4 days. The mean concentration of ozone over a 2-day period was associated with a 1.8% increase in mortality from cardiovascular diseases. NO2 was not consistently related to mortality. Fine particles had an independent effect on mortality when modeled simultaneously with other pollutants, and the association of ozone with cardiovascular mortality was strengthened after adjusting for NO2 and PM2.5. These results support previous findings that urban air pollution at current levels leads to excess mortality and suggest that fine particles may play a causal role in producing that excess.
PMCID: PMC1533229  PMID: 9831546
14.  Effects of ozone and other pollutants on the pulmonary function of adult hikers. 
This study evaluated the acute effects of ambient ozone (O3), fine particulate matter (PM2.5), and strong aerosol acidity on the pulmonary function of exercising adults. During the summers of 1991 and 1992, volunteers (18-64 years of age) were solicited from hikers on Mt. Washington, New Hampshire. Volunteer nonsmokers with complete covariates (n = 530) had pulmonary function measured before and after their hikes. We calculated each hiker's posthike percentage change in forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), the ratio of these two (FEV1/FVC), forced expiratory flow between 25 and 75% of FVC(FEF25-75%), and peak expiratory flow rate (PEFR). Average O3 exposures ranged from 21 to 74 ppb. After adjustment for age,sex, smoking status (former versus never), history of asthma or wheeze, hours hiked, ambient temperature, and other covariates, there was a 2.6% decline in FEV1 [95% confidence interval (CI), 0.4-4.7; p = 0.02] and a 2.2% decline in FVC (CI, 0.8-3.5; p =0.003) for each 50 ppb increment in mean O3. There were consistent associations of decrements in both FVC (0.4% decline; CI,0.2-0.6, p = 0.001) and PEFR (0.8% decline; CI, 0.01-1.6; p = 0.05) with PM2.5 and of decrements in PEFR (0.4% decline; CI, 0.1-0.7; p = 0.02) with strong aerosol acidity across the interquartile range of these exposures. Hikers with asthma or a history of wheeze (n = 40) had fourfold greater responsiveness to ozone than others. With prolonged outdoor exercise, low-level exposures to O3, PM2.5, and strong aerosol acidity were associated with significant effects on pulmonary function among adults. Hikers with a history of asthma or wheeze had significantly greater air pollution-related changes in pulmonary function.
PMCID: PMC1533017  PMID: 9435151

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