Introduction

Exposure to secondhand smoke (SHS) is influenced by norms and regulations, socioeconomic status and immediate personal interactions. SHS exposure may occur in various settings, including the living space, workplace, and other social environments. This study examines the association between exposure to SHS and nicotine dependence among smokers.

Methods

A cross-sectional sample of 246 Black (60% male and 40% female) current smokers age 40 and older, from Baltimore, Maryland and Washington, D.C, responded to an interviewer-administered questionnaire. We examined nicotine dependence using clinical guidelines based on the Diagnostic and Statistical Manual of Mental Disorders, Text Revision (2000). We performed multivariate logistic regression to assess the association between SHS and nicotine dependence.

Results

SHS exposure in the current home environment and exposure in settings outside the home as well as difficulty to quit smoking and heaviness of smoking were associated with nicotine dependence. After adjustment for age, gender, education, income, employment status, current alcohol consumption, history of marijuana use, and number of cigarettes smoked per day; exposure to SHS at home only, and in both current home environments and other settings, continued to be associated with clinically-defined levels nicotine dependence (OR = 2.25; 95% CI 1.05, 4.86 vs. OR = 2.31; 95% CI 1.03, 5.18), respectively.

Discussion

These findings highlight the relative importance of examining SHS exposure in personal (residential and automobile) and public (workplace and outdoor) settings by current smokers. Promotion of smoke-free environments may reduce the prevalence of nicotine dependence among current smokers.

Background: Diabetes affects an estimated 346 million persons globally, and total deaths from diabetes are projected to increase > 50% in the next decade. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. In 2011, the National Toxicology Program (NTP) organized a workshop to assess the literature for evidence of associations between certain chemicals, including inorganic arsenic, and diabetes and/or obesity to help develop a focused research agenda. This review is derived from discussions at that workshop.

Objectives: Our objectives were to assess the consistency, strength/weaknesses, and biological plausibility of findings in the scientific literature regarding arsenic and diabetes and to identify data gaps and areas for future evaluation or research. The extent of the existing literature was insufficient to consider obesity as an outcome.

Data Sources, Extraction, and Synthesis: Studies related to arsenic and diabetes or obesity were identified through PubMed and supplemented with relevant studies identified by reviewing the reference lists in the primary literature or review articles.

Conclusions: Existing human data provide limited to sufficient support for an association between arsenic and diabetes in populations with relatively high exposure levels (≥ 150 µg arsenic/L in drinking water). The evidence is insufficient to conclude that arsenic is associated with diabetes in lower exposure (< 150 µg arsenic/L drinking water), although recent studies with better measures of outcome and exposure support an association. The animal literature as a whole was inconclusive; however, studies using better measures of diabetes-relevant end points support a link between arsenic and diabetes.

Background

Methylmercury (MeHg) is a neurotoxin primarily found in seafood; exposures in reproductive-age women are of concern due to vulnerability of the developing fetus. MeHg is mainly eliminated via an enterohepatic cycle involving the liver and gallbladder. Dysfunction in these organs has been associated with slower MeHg elimination in laboratory animals. We hypothesized that women testing positive for chronic hepatitis B (HBV) or C (HCV), both associated with risk of longer-term liver and gallbladder impairment, would have higher total blood mercury (TBHg) concentrations than those negative for the viruses, reflecting slower MeHg elimination.

Methods

Geometric mean (GM) TBHg levels from a representative sample of over 5,000 seafood-consuming, reproductive-age women from eight years (2001–2008) of the US NHANES survey were compared by viral hepatitis status (as determined by serological assay) using multiple linear regression. Adjustment was made for estimated MeHg intake from seafood consumption, social and demographic variables and other predictors.

Results

Women with chronic HBV had 1.52 (95% CI 1.13, 2.05, p < 0.01) times the GM TBHg of women who had not come into contact with the virus. The positive association was strongest in those with most severe disease. A modest negative association was found with HCV markers.

Conclusions

While study design prevents inferences on causality, the finding that MeHg biomarkers differ by hepatitis status in this population suggests viral hepatitis may alter the pace of MeHg elimination. Offspring of HBV-infected seafood-consuming women may be at higher risk of MeHg-induced developmental delays than offspring of those uninfected. Possible reasons for the unanticipated negative association with HCV are explored.

Background. Low-level lead exposure is widespread and has been implicated as a chronic kidney disease (CKD) risk factor. However, studies evaluating associations of lead dose with newer, potentially more accurate, estimates of kidney function, in participants with a wide range of glomerular filtration rates (GFRs), are scarce.

Methods. We compared associations of blood lead and estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease (MDRD), Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and cystatin C single variable, multivariable and combined creatinine/cystatin C equations in 3941 adults who participated in the 1999–2002 National Health and Nutrition Examination Survey cystatin C subsample.

Results. Geometric mean blood lead was 1.7 μg/dL. After multivariable adjustment, differences [95% confidence interval (CI)] in mean eGFR for a doubling of blood lead were −1.9 (−3.2, −0.7), −1.7 (−3.0, −0.5) and −1.4 (−2.3, −0.5) mL/min/1.73 m2, using the cystatin C single variable, multivariable and combined creatinine/cystatin C equations, respectively, reflecting lower eGFR with increased blood lead. The corresponding differences (95% CI) were −0.9 (−1.9, 0.02) and −0.9 (−1.8, 0.01) using the creatinine-based MDRD and CKD-EPI equations, respectively. In participants aged ≥60 years, differences in mean eGFR ranged from −3.0 to −4.5 mL/min/1.73 m2, and odds of reduced eGFR (<60 mL/min/1.73 m2) were increased for all estimates of GFR.

Conclusions. These results support the inclusion of cystatin C-based eGFR in future lead research and provide additional evidence for environmental lead exposure as a CKD risk factor.

Background

High chronic exposure to inorganic arsenic may contribute to the development of hypertension. Limited information is available, however, on the association of low to moderate exposure to inorganic arsenic with blood pressure levels and hypertension. We investigated the association of exposure to inorganic arsenic (as measured in urine) with systolic and diastolic blood pressure levels and the prevalence of hypertension in U.S. adults.

Methods

We studied 4167 adults 20 years of age or older who participated in the National Health and Nutrition Examination Survey (NHANES) from 2003 through 2008 and for whom total arsenic, dimethylarsinate (DMA) and arsenobetaine had been assessed in urine.

Results

The median (inter-quartile range) urine concentrations were 8.3 μg/L (4.2– 17.1) for total arsenic, 3.6 μg/L (2.0– 6.0) for DMA and 1.4 μg/L (0.3– 6.3) for arsenobetaine. The weighted prevalence of hypertension in the study population was 36%. After multivariable adjustment, a 2-fold increase in total arsenic was associated with a hypertension odds ratio of 0.98 (95% confidence interval = 0.86 to 1.11). A doubling of total arsenic minus arsenobetaine was associated with a hypertension OR of 1.03 (0.94 to 1.14) and a doubling of DMA concentrations was associated with a hypertension OR of 1.11 (0.99 to 1.24). Total arsenic, total arsenic minus arsenobetaine, or DMA levels were not associated with systolic or diastolic blood pressure.

Conclusions

At the low to moderate levels typical of the U.S. population, total arsenic, total arsenic minus arsenobetaine, and DMA concentrations in urine were not associated with the prevalence of hypertension or with systolic or diastolic blood pressure levels. A weak association of DMA with hypertension could not be ruled out.

Background: Urine cadmium concentrations were associated with all-cause and cardiovascular mortality in men in the 1988–1994 U.S. National Health and Nutrition Examination Survey (NHANES) population. Since 1988, cadmium exposure has decreased substantially in the United States. The associations between blood and urine cadmium and cardiovascular disease (CVD) mortality at more recent levels of exposure are unknown.

Objectives: We evaluated the prospective association of blood and urine cadmium concentrations with all-cause and CVD mortality in the 1999–2004 U.S. population.

Methods: We followed 8,989 participants who were ≥ 20 years of age for an average of 4.8 years. Hazard ratios for mortality end points comparing the 80th to the 20th percentiles of cadmium distributions were estimated using Cox regression.

Results: The multivariable adjusted hazard ratios [95% confidence intervals (CIs)] for blood and urine cadmium were 1.50 (95% CI: 1.07, 2.10) and 1.52 (95% CI: 1.00, 2.29), respectively, for all-cause mortality, 1.69 (95% CI: 1.03, 2.77) and 1.74 (95% CI: 1.07, 2.83) for CVD mortality, 1.98 (95% CI: 1.11, 3.54) and 2.53 (95% CI: 1.54, 4.16) for heart disease mortality, and 1.73 (95% CI: 0.88, 3.40) and 2.09 (95% CI: 1.06, 4.13) for coronary heart disease mortality. The population attributable risks associated with the 80th percentile of the blood (0.80 μg/L) and urine (0.57 μg/g) cadmium distributions were 7.0 and 8.8%, respectively, for all-cause mortality and 7.5 and 9.2%, respectively, for CVD mortality

Conclusions: We found strongly suggestive evidence that cadmium, at substantially low levels of exposure, remains an important determinant of all-cause and CVD mortality in a representative sample of U.S. adults. Efforts to further reduce cadmium exposure in the population could contribute to a substantial decrease in CVD disease burden.

Exposure to high inorganic arsenic concentrations in drinking water has been related to detrimental health effects, including cancers and possibly cardiovascular disease, in many epidemiological studies. Recent studies suggest that arsenic might elicit some of its toxic effects also at lower concentrations. The Strong Heart Study, a large epidemiological study of cardiovascular disease in American Indian communities, collected urine samples and performed medical examinations on 4,549 participants over a 10-year period beginning in 1989. We used anion-exchange HPLC/ICPMS to determine concentrations of arsenic species (methylarsonate, dimethylarsinate and arsenate) in 5,095 urine samples from the Strong Heart Study. We repeated the chromatography on a portion of the urine sample that had been oxidised, by addition of H2O2, to provide additional information on the presence of As(III) species and thio-arsenicals, and by difference, of arsenobetaine and other non-retained cations. Total concentrations for As, Cd, Mo, Pb, Sb, Se, U, W, and Zn were also determined in the urine samples by ICPMS. The dataset will be used to evaluate the relationships between the concentrations of urinary arsenic species and selected metals with various cardiometabolic health endpoints. We present and discuss the analytical protocol put in place to produce this large and valuable dataset.

Background: Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas.

Objective: We summarized published epidemiologic studies concerning arsenic exposure and hypertension or blood pressure (BP) measurements to evaluate the potential relationship.

Data sources and extraction: We searched PubMed, Embase, and TOXLINE and applied predetermined exclusion criteria. We identified 11 cross-sectional studies from which we abstracted or derived measures of association and calculated pooled odds ratios (ORs) using inverse-variance weighted random-effects models.

Data synthesis: The pooled OR for hypertension comparing the highest and lowest arsenic exposure categories was 1.27 [95% confidence interval (CI): 1.09, 1.47; p-value for heterogeneity = 0.001; I2 = 70.2%]. In populations with moderate to high arsenic concentrations in drinking water, the pooled OR was 1.15 (95% CI: 0.96, 1.37; p-value for heterogeneity = 0.002; I2 = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I2 = 46.6%) before and after excluding an influential study, respectively. The corresponding pooled OR in populations with low arsenic concentrations in drinking water was 1.56 (95% CI: 1.21, 2.01; p-value for heterogeneity = 0.27; I2 = 24.6%). A dose–response assessment including six studies with available data showed an increasing trend in the odds of hypertension with increasing arsenic exposure. Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings.

Conclusion: In this systematic review we identified an association between arsenic and the prevalence of hypertension. Interpreting a causal effect of environmental arsenic on hypertension is limited by the small number of studies, the presence of influential studies, and the absence of prospective evidence. Additional evidence is needed to evaluate the dose–response relationship between environmental arsenic exposure and hypertension.

Background: Public health policies such as tobacco control, air pollution reduction, and hazardous waste remediation may have reduced cadmium exposure among U.S. adults. However, trends in urine cadmium, a marker of cumulative cadmium exposure, have not been evaluated.

Objectives: We estimated the trends in urine cadmium concentrations in U.S. adults using data from the National Health and Nutrition Examination Surveys (NHANES) from 1988 to 2008. We also evaluated the impact of changes in the distribution of available cadmium determinants (age, sex, race, education, body mass index, smoking, and occupation) at the population level to explain cadmium trends.

Methods: The study population included 19,759 adults ≥ 20 years of age with measures of urine cadmium and cadmium determinants.

Results: Age-adjusted geometric means of urine cadmium concentrations were 0.36, 0.35, 0.27, 0.27, 0.28, 0.25, and 0.26 µg/g creatinine in 1988–1991, 1991–1994, 1999–2000, 2001–2002, 2003–2004, 2005–2006, and 2007–2008, respectively. The age, sex, and race/ethnicity-adjusted percent reduction in urine cadmium geometric means comparing 1999–2002 and 2003–2008 with 1988–1994 were 27.8% (95% confidence interval: 22.3%, 32.9%) and 34.3% (29.9%, 38.4%), respectively (p-trend < 0.001), with reductions in all participant subgroups investigated. In never smokers, reductions in serum cotinine accounted for 15.6% of the observed reduction. In ever smokers, changes in smoking cessation, and cumulative and recent dose accounted for 17.1% of the observed reduction.

Conclusions: Urine cadmium concentrations decreased markedly between 1988 and 2008. Declining smoking rates and changes in exposure to tobacco smoke may have played an important role in the decline of urine cadmium concentrations, benefiting both smokers and nonsmokers. Cadmium has been associated to several health outcomes in NHANES 1999–2008. Consequently, despite the observed decline, further reduction in cadmium exposure is needed.

Background

Seafood is the main source of organic arsenic exposure (arsenobetaine, arsenosugars and arsenolipids) in the population. Arsenosugars and arsenolipids are metabolized to several species including dimethylarsinate (DMA).

Objective

Evaluate the association of seafood intake with spot urine arsenic concentrations in the 2003–2006 National Health Nutrition and Examination Survey (NHANES).

Methods

We studied 4276 participants ≥6 y. Total arsenic was measured using inductively coupled plasma dynamic reaction cell mass spectrometry (ICPMS). Urine DMA and arsenobetaine were measured by high-performance liquid chromatography coupled with ICPMS.

Results

Participants reporting seafood in the past 24-h had higher urine concentrations of total arsenic (median 24.5 vs. 7.3 µg/L), DMA (6.0 vs. 3.5 µg/L), arsenobetaine (10.2 vs. 0.9 µg/L) and total arsenic minus arsenobetaine (11.0 vs. 5.5 µg/L). Participants reporting seafood ≥2/wk vs. never during the past year had 2.3 (95% confidence interval 1.9, 2.7), 1.4 (1.2, 1.6), 6.0 (4.6, 7.8) and 1.7 (1.4, 2.0) times higher (p-trend <0.001) concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine, respectively. In participants without detectable arsenobetaine and in analyses adjusted for arsenobetaine, seafood consumption in the past year was not associated with total arsenic or DMA concentrations in urine.

Conclusion

Seafood intake was a major determinant of increased urine concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine in the US population. Epidemiologic studies that use total arsenic, DMA, the sum of inorganic arsenic, methylarsonate and DMA, and total arsenic minus arsenobetaine as markers of inorganic arsenic exposure and/or metabolism need to address seafood intake.

Background: Cadmium is a nephrotoxicant at high exposure levels. Few studies have evaluated the role of cadmium in kidney function at low-exposure levels.

Objective: We evaluated the association of blood cadmium with estimated glomerular filtration rate (eGFR) in the Korean adult population.

Methods: We evaluated 1,909 adults ≥ 20 years of age who participated in the 2005 Korean National Health and Nutrition Examination Survey and had blood cadmium determinations. eGFR was calculated using the Modification of Diet in Renal Disease equation.

Results: Blood cadmium geometric means were 1.57 μg/L for men and 1.49 μg/L for women. The difference in eGFR levels that compared participants in the highest versus lowest cadmium tertiles, after multivariable adjustment, was –1.85 [95% confidence interval (CI): –3.55, –0.16] mL/min per 1.73 m2 in women and 0.67 (–1.16, 2.50) mL/min per 1.73 m2 in men. Among men, the association between blood cadmium and eGFR was modified by blood lead levels (p-value for interaction = 0.048). The fully adjusted differences in eGFR levels for a 2-fold increase in blood cadmium levels were –1.14 (–3.35, 1.07) and 1.84 (0.54, 3.14) mL/min per 1.73 m2 in men with blood lead levels below and above the median (2.75 μg/dL), respectively.

Conclusion: Elevated blood cadmium levels were associated with lower eGFR in women, which supports the role of cadmium as a risk factor for chronic kidney disease. In men, there was no overall association, although elevated blood cadmium levels were associated with higher eGFR levels in men with high blood lead levels and nonstatistically associated with lower eGFR levels in men with low blood lead levels.

Gender differences in the association of blood and urine cadmium concentrations with peripheral arterial disease (PAD) were evaluated by using data from 6,456 US adults aged ≥40 years who participated in the 1999–2004 National Health and Nutrition Examination Survey. PAD was defined as an ankle-brachial blood pressure index of <0.9 in at least one leg. For men, the adjusted odds ratios for PAD comparing the highest with the lowest quintiles of blood and urine cadmium concentrations were 1.82 (95% confidence interval (CI): 0.82, 4.05) and 4.90 (95% CI: 1.55, 15.54), respectively, with a progressive dose-response relation and no difference by smoking status. For women, the corresponding odds ratios were 1.19 (95% CI: 0.66, 2.16) and 0.56 (95% CI: 0.18, 1.71), but there was evidence of effect modification by smoking: among women ever smokers, there was a positive, progressive dose-response relation; among women never smokers, there was a U-shaped dose-response relation. Higher blood and urine cadmium levels were associated with increased prevalence of PAD, but women never smokers showed a U-shaped relation with increased prevalence of PAD at very low cadmium levels. These findings add to the concern of increased cadmium exposure as a cardiovascular risk factor in the general population.

OBJECTIVE

High selenium has been recently associated with several cardiovascular and metabolic risk factors including diabetes, blood pressure and lipid levels. We evaluated the association of serum selenium with fasting serum lipid levels in the National Health and Nutrition Examination Survey (NHANES) 2003–2004, the most recently available representative sample of the US population that measured selenium levels.

METHODS

Cross-sectional analysis of 1159 adults ≥40 years old from NHANES 2003–2004. Serum selenium was measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry. Fasting serum total-cholesterol, triglycerides, and HDL cholesterol were measured enzymatically and LDL cholesterol was calculated.

RESULTS

Mean serum selenium was 136.7 µg/L. The multivariable adjusted average differences (95% confidence interval) comparing the highest (≥147 µg/L) to the lowest (<124 µg/L) selenium quartiles were 18.9 (9.9, 28.0) mg/dL for total cholesterol, 12.7 (3.3, 22.2) mg/dL for LDL cholesterol, 3.9 (0.4, 7.5) mg/dL for HDL cholesterol, and 11.5 (−7.6, 30.7) mg/dL for triglycerides. In spline regression models, total and LDL cholesterol levels increased progressively with increasing selenium concentrations. HDL cholesterol increased with selenium but reached a plateau above 120 µg/L of serum selenium (20th percentile). The triglyceride-selenium relationship was U-shaped.

CONCLUSION

In US adults, high serum selenium concentrations were associated with increased serum concentrations of total and LDL cholesterol. Selenium was associated with increasing HDL cholesterol only at low selenium levels. Given increasing trends in dietary selenium intake and supplementation, the causal mechanisms underlying these associations need to be fully characterized.

Background

Lead exposure is associated with elevated blood pressure during pregnancy; however, the magnitude of this relationship at low exposure levels is unclear.

Objectives

Our goal was to determine the association between low-level lead exposure and blood pressure during late pregnancy.

Methods

We collected admission and maximum (based on systolic) blood pressures during labor and delivery among 285 women in Baltimore, Maryland. We measured umbilical cord blood lead using inductively coupled plasma mass spectrometry. Multivariable models were adjusted for age, race, median household income, parity, smoking during pregnancy, prepregnancy body mass index, and anemia. These models were used to calculate benchmark dose values.

Results

Geometric mean cord blood lead was 0.66 μg/dL (95% confidence interval, 0.61–0.70). Comparing blood pressure measurements between those in the highest and those in the lowest quartile of lead exposure, we observed a 6.87-mmHg (1.51–12.21 mmHg) increase in admission systolic blood pressure and a 4.40-mmHg (0.21–8.59 mmHg) increase in admission diastolic blood pressure after adjustment for confounders. Corresponding values for maximum blood pressure increase were 7.72 (1.83–13.60) and 8.33 (1.14–15.53) mmHg. Benchmark dose lower limit values for a 1-SD increase in blood pressure were < 2 μg/dL blood lead for all blood pressure end points.

Conclusions

A significant association between low-level lead exposures and elevations in maternal blood pressure during labor and delivery can be observed at umbilical blood lead levels < 2 μg/dL.

Rationale: Nuclear factor erythroid 2–related factor 2 (Nrf2), an important regulator of lung antioxidant defenses, declines in chronic obstructive pulmonary disease (COPD). However, Nrf2 also regulates the proteasome system that degrades damaged and misfolded proteins. Because accumulation of misfolded proteins in the endoplasmic reticulum (ER) causes ER stress and ER stress-induced apoptosis, Nrf2 may potentially prevent ER stress-mediated apoptosis in COPD.

Objectives: To determine whether Nrf2-regulated proteasome function affects ER stress-mediated apoptosis in COPD.

Methods: We assessed the expression of Nrf2, Nrf2-dependent proteasomal subunits, proteasomal activity, markers of ER stress, and apoptosis in emphysematous lungs of mice exposed to cigarette smoke (CS) as well as peripheral lung tissues from normal control subjects and patients with COPD.

Measurements and Main Results: Compared with wild-type mice, emphysematous lungs of CS-exposed Nrf2-deficient mice exhibited markedly lower proteasomal activity and elevated markers of ER stress and apoptosis. Furthermore, compared with normal control subjects, lungs of patients with mild and advanced COPD showed a marked decrease in the expression of Nrf2-regulated proteasomal subunits and total proteasomal activity. However, they were associated with greater levels of ER stress and apoptosis markers. In vitro studies have demonstrated that enhancing proteasomal activity in Beas2B cells either by sulforaphane, an activator of Nrf2, or overexpression of Nrf2-regulated proteasomal subunit PSMB6, significantly inhibited cigarette smoke condensate (CSC)-induced ER stress and cell death.

Conclusions: Impaired Nrf2 signaling causes significant decline in proteasomal activity and heightens ER stress response in lungs of patients with COPD and CS-exposed mice. Accordingly, pharmacological approaches that augment Nrf2 activity may protect against COPD progression by both up-regulating antioxidant defenses and relieving ER stress.

Environmental cadmium and lead exposures are widespread, and both metals are nephrotoxic at high exposure levels. Few studies have evaluated the associations between low-level cadmium and clinical renal outcomes, particularly with respect to joint cadmium and lead exposure. The geometric mean levels of blood cadmium and lead were 0.41 μg/L (3.65 nmol/L) and 1.58 μg/dL (0.076 μmol/L), respectively, in 14,778 adults aged ≥20 years who participated in the National Health and Nutrition Examination Survey (1999–2006). After adjustment for survey year, sociodemographic factors, chronic kidney disease risk factors, and blood lead, the odds ratios for albuminuria (≥30 mg/g creatinine), reduced estimated glomerular filtration rate (eGFR) (<60 mL/minute/1.73 m2), and both albuminuria and reduced eGFR were 1.92 (95% confidence interval (CI): 1.53, 2.43), 1.32 (95% CI: 1.04, 1.68), and 2.91 (95% CI: 1.76, 4.81), respectively, comparing the highest with the lowest blood cadmium quartiles. The odds ratios comparing participants in the highest with the lowest quartiles of both cadmium and lead were 2.34 (95% CI: 1.72, 3.18) for albuminuria, 1.98 (95% CI: 1.27, 3.10) for reduced eGFR, and 4.10 (95% CI: 1.58, 10.65) for both outcomes. These findings support consideration of cadmium and lead as chronic kidney disease risk factors in the general population and provide novel evidence of risk with environmental exposure to both metals.

Background

Secondhand tobacco smoke (SHS) exposure is a global public health problem. Ghana currently has no legislation to prevent smoking in public places. To provide data on SHS levels in hospitality venues in Ghana the authors measured (1) airborne particulate matter <2.5 μm (PM2.5) and nicotine concentrations and (2) hair nicotine concentrations in non-smoking employees. Quantifying SHS exposure will provide evidence needed to develop tobacco control legislation.

Method

PM2.5 was measured for 30 min in 75 smoking and 13 non-smoking venues. Air nicotine concentrations were measured for 7 days in 8 smoking and 2 non-smoking venues. Additionally, 63 non-smoking employees provided hair samples for nicotine analysis.

Result

Compared to non-smoking venues, smoking venues had markedly elevated PM2.5 (median 553 [IQR 259–1038] vs 16.0 [14.0–17.0] μg/m3) and air nicotine (1.83 [0.91–4.25] vs 0.03 [0.02–0.04] μg/m3) concentrations. Hair nicotine concentrations were also higher in non-smoking employees working in smoking venues (median 2.49 [0.46–6.84] ng/mg) compared to those working in non-smoking venues (median 0.16 [0.08–0.79] ng/mg). Hair nicotine concentrations correlated with self-reported hours of SHS exposure (r=0.35), indoor air PM2.5 concentrations (r=0.47) and air nicotine concentrations (r=0.63).

Conclusion

SHS levels were unacceptably high in public places in Ghana where smoking is allowed, despite a relatively low-smoking prevalence in the country. This is one of the first studies to ascertain SHS and hair nicotine in Africa. Levels were comparable to those measured in American, Asian and European countries without or before smoking bans. Implementing a comprehensive smoke-free legislation that protects workers and customers from exposure to secondhand smoke is urgently needed in Ghana.

Objective

To compare air nicotine concentrations according to the smoking policy selected by bars/restaurants in Santiago, Chile before and after the enactment of partial smoking ban legislation in 2007 (establishments could be smoke free, have segregated (mixed) smoking and non-smoking areas, or allow smoking in all areas).

Methods

The study measured air nicotine concentrations over 7 days to characterise secondhand smoke exposure in 30 bars/restaurants in 2008. Owner/manager interviews and physical inspections were conducted.

Results

Median IQR air nicotine concentrations measured in all venues were 4.38 (0.61–13.62) μg/m3. Air nicotine concentrations were higher in bars (median 7.22, IQR 2.48–15.64 μg/m3) compared to restaurants (1.12, 0.15–9.22 μg/m3). By smoking status, nicotine concentrations were higher in smoking venues (13.46, 5.31–16.87 μg/m3), followed by smoking areas in mixed venues (9.22, 5.09–14.90 μg/m3) and non-smoking areas in mixed venues (0.99, 0.19–1.27 μg/m3). Air nicotine concentrations were markedly lower in smoke-free venues (0.12, 0.11–0.46 μg/m3). After adjustment for differences in volume and ventilation, air nicotine concentrations were 3.2, 35.5 and 56.2 times higher in non-smoking areas in mixed venues, smoking areas in mixed venues and smoking venues, respectively, compared to smoke-free venues.

Conclusions

Exposure to secondhand smoke remains high in bars and restaurants in Santiago, Chile. These findings demonstrate that the partial smoking ban legislation enacted in Chile in 2007 provides no protection to employees working in those venues. Enacting a comprehensive smoke-free legislation which protects all people from exposure to secondhand smoke in all public places and workplaces is urgently needed.

Background

Selenium is an antioxidant micronutrient with potential interest for cardiovascular disease prevention. Few studies have evaluated the association between selenium and hypertension, with inconsistent findings. We explored the relationship of serum selenium concentrations with blood pressure and hypertension in a representative sample of the US population.

Methods and Results

Cross-sectional analysis of 2,638 adults ≥40 year old who participated in the National Health and Nutrition Examination Survey (NHANES) 2003–2004. Serum selenium was measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry. Hypertension was defined as blood pressure ≥140/90 mmHg or current use of antihypertensive medication. Mean serum selenium was 137.1 µg/L. The multivariable adjusted differences (95% confidence interval) in blood pressure levels comparing the highest (≥150 µg/L) to the lowest (<122 µg/L) quintile of serum selenium were 4.3 (1.3, 7.4), 1.6 (−0.5, 3.7) and 2.8 (0.8, 4.7) mmHg for systolic, diastolic, and pulse pressure, respectively. The corresponding odds ratio (95% CI) for hypertension was 1.73 (1.18, 2.53). In spline regression models, blood pressure levels and the prevalence of hypertension increased with increasing selenium concentrations up to 160 µg/L.

Conclusions

High serum selenium concentrations were associated with higher prevalence of hypertension. These findings call for a thorough evaluation of the risks and benefits associated with high selenium status in the US.

The authors conducted a cross-sectional study of the association of serum selenium with the prevalence of peripheral arterial disease among 2,062 US men and women 40 years of age or older participating in the National Health and Nutrition Examination Survey, 2003–2004. Serum selenium was measured by using inductively coupled plasma-dynamic reaction cell-mass spectrometry. Peripheral arterial disease was defined as an ankle-brachial blood pressure index <0.90. The age-, sex-, and race-adjusted prevalence of peripheral arterial disease decreased with increasing serum selenium (P for linear trend = 0.02), but there was an indication of an upturn in risk in the highest quartile of serum selenium. The fully adjusted odds ratios for peripheral arterial disease comparing selenium quartiles 2, 3, and 4 with the lowest quartile were 0.75 (95% confidence interval: 0.37, 1.52), 0.58 (95% confidence interval: 0.28, 1.19), and 0.67 (95% confidence interval: 0.34, 1.31), respectively. In spline regression models, peripheral arterial disease prevalence decreased with increasing serum selenium levels up to 150–160 ng/mL, followed by a gradual increase at higher selenium levels. The association between serum selenium levels and the prevalence of peripheral arterial disease was not statistically significant, although a U-shaped relation was suggested.

The aim of this study was to assess the levels of secondhand smoke (SHS) exposure of men and women in public places in Kyrgyzstan. This cross-sectional study involved 10 bars and restaurants in Bishkek the capital city of Kyrgyzstan. Smoking was allowed in all establishments. Median (interquartile range) air nicotine concentrations were 6.82 (2.89, 8.86) μg/m3. Employees were asked about their smoking history and exposure to SHS at work. Employees were exposed to SHS for mean (SD) 13.5 (3.6) hours a day and 5.8 (1.4) days a week. Women were exposed to more hours of SHS at work compared to men. Hospitality workers are exposed to excessive amounts of SHS from customers. Legislation to ban smoking in public places including bars and restaurants is urgently needed to protect workers and patrons from the harmful effects of SHS.

Oxidative stress results in protein oxidation and is involved in the pathogenesis of lung diseases such as chronic obstructive pulmonary disorder (COPD). Sulfiredoxin-1 (Srx1) catalyzes reduction of cysteine sulfinic acid to sulfenic acid in oxidized proteins and protects them from inactivation. This study examined the mechanism of transcriptional regulation of Srx1 and its possible protective role during oxidative stress associated with COPD. Nrf2, a transcription factor known to influence susceptibility to pulmonary diseases, upregulates Srx1 expression during oxidative stress caused by cigarette smoke exposure in the lungs of mice. Disruption of Nrf2 signaling by genetic knockout in mice or RNAi in cells downregulated the expression of Srx1. In silico analysis of the 5′-promoter flanking region of Srx1 identified multiple antioxidant response elements that are highly conserved. Reporter and chromatin-immunoprecipation assays demonstrated that ARE1 at −228 is critical for the Nrf2-mediated response. Attenuation of Srx1 expression with RNAi potentiated the toxicity of hydrogen peroxide (H2O2), whereas overexpression of Srx1 protected against H2O2 mediated cell death in vitro. Immunoblot analysis revealed dramatic decreases in Srx1 expression in lungs from patients with COPD relative to non-emphysematous lungs together with a decline in Nrf2 protein. Thus, Srx1, a key Nrf2-regulated gene, contributes to protection against oxidative injury in the lung.

Objective

To assess airborne nicotine concentrations as an indicator of second‐hand smoke (SHS) exposure in public places in both urban and rural areas of China.

Design

Measurement of vapour‐phase nicotine concentration using a common protocol in all locations. A total of 273 samplers were placed for 7 days in urban and rural areas of China, including Beijing and the capital city, and a county (rural) area of the following provinces: Sichuan (Chengdu/Mianzhu), Jiangxi (Nanchang/Anyi) and Henan (Zhengzhou/Xin'an).

Setting

Samplers were placed in hospitals, secondary schools, city government buildings, train stations, restaurants and entertainment establishments (internet cafes, mahjong parlours and karaoke bars) in each location.

Main outcome measure

The time‐weighted average airborne concentration of nicotine (μg/m3) was measured by gas chromatography.

Results

Airborne nicotine was detected in 91% of the locations sampled. Beijing had the highest nicotine concentrations in most indoor environments (median 3.01 μg/m3) and Chengdu had the lowest concentrations (median 0.11 μg/m3). Overall, restaurants and entertainment establishments had the highest nicotine concentrations (median 2.17 and 7.48 μg/m3, respectively). High nicotine concentrations were also found in government buildings and in train stations.

Conclusions

The data collected in this study provide evidence that SHS exposure is frequent in public places in China. Environmental nicotine concentrations in China provide evidence for implementation and enforcement of smoke‐free initiatives in public places in China and indicate the need for protecting the public from exposure to SHS.

Rationale: Oxidative stress is a key contributor in chronic obstructive pulmonary disease (COPD) pathogenesis caused by cigarette smoking. NRF2, a redox-sensitive transcription factor, dissociates from its inhibitor, KEAP1, to induce antioxidant expression that inhibits oxidative stress.

Objectives: To determine the link between severity of COPD, oxidative stress, and NRF2-dependent antioxidant levels in the peripheral lung tissue of patients with COPD.

Methods: We assessed the expression of NRF2, NRF2-dependent antioxidants, regulators of NRF2 activity, and oxidative damage in non-COPD (smokers and former smokers) and smoker COPD lungs (mild and advanced). Cigarette smoke–exposed human lung epithelial cells (Beas2B) and mice were used to understand the mechanisms.

Measurements and Main Results: When compared with non-COPD lungs, the COPD patient lungs showed (1) marked decline in NRF2-dependent antioxidants and glutathione levels, (2) increased oxidative stress markers, (3) significant decrease in NRF2 protein with no change in NRF2 mRNA levels, and (4) similar KEAP1 but significantly decreased DJ-1 levels (a protein that stabilizes NRF2 protein by impairing KEAP1-dependent proteasomal degradation of NRF2). Exposure of Bea2B cells to cigarette smoke caused oxidative modification and enhanced proteasomal degradation of DJ-1 protein. Disruption of DJ-1 in mouse lungs, mouse embryonic fibroblasts, and Beas2B cells lowered NRF2 protein stability and impaired antioxidant induction in response to cigarette smoke. Interestingly, targeting KEAP1 by siRNA or the small-molecule activator sulforaphane restored induction of NRF2-dependent antioxidants in DJ-1–disrupted cells in response to cigarette smoke.

Conclusions: NRF2-dependent antioxidants and DJ-1 expression was negatively associated with severity of COPD. Therapy directed toward enhancing NRF2-regulated antioxidants may be a novel strategy for attenuating the effects of oxidative stress in the pathogenesis of COPD.