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  1. van de Merwe JP, Hodge M, Olszowy HA, Whittier JM, Ibrahim K, Lee SY
    Environ Health Perspect, 2009 Sep;117(9):1397-401.
    PMID: 19750104 DOI: 10.1289/ehp.0900813
    Persistent organic pollutants (POPs)-such as organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs)-and heavy metals have been reported in sea turtles at various stages of their life cycle. These chemicals can disrupt development and function of wildlife. Furthermore, in areas such as Peninsular Malaysia, where the human consumption of sea turtle eggs is prevalent, egg contamination may also have public health implications.
  2. McDaniel PA, Solomon G, Malone RE
    Environ Health Perspect, 2005 Dec;113(12):1659-65.
    PMID: 16330343
    Tobacco is a heavily pesticide-dependent crop. Because pesticides involve human safety and health issues, they are regulated nationally and internationally; however, little is known about how tobacco companies respond to regulatory pressures regarding pesticides. In this study we analyzed internal tobacco industry documents to describe industry activities aimed at influencing pesticide regulations. We used a case study approach based on examination of approximately 2,000 internal company documents and 3,885 pages of U.S. Environmental Protection Agency documents obtained through Freedom of Information Act requests. The cases involved methoprene, the ethylene bisdithiocarbamates, and phosphine. We show how the tobacco industry successfully altered the outcome in two cases by hiring ex-agency scientists to write reports favorable to industry positions regarding pesticide regulations for national (U.S. Environmental Protection Agency) and international (World Health Organization) regulatory bodies. We also show how the industry worked to forestall tobacco pesticide regulation by attempting to self-regulate in Europe, and how Philip Morris encouraged a pesticide manufacturer to apply for higher tolerance levels in Malaysia and Europe while keeping tobacco industry interest a secret from government regulators. This study suggests that the tobacco industry is able to exert considerable influence over the pesticide regulatory process and that increased scrutiny of this process and protection of the public interest in pesticide regulation may be warranted.
  3. Liu W, Zhang J, Hashim JH, Jalaludin J, Hashim Z, Goldstein BD
    Environ Health Perspect, 2003 Sep;111(12):1454-60.
    PMID: 12948883
    Burning mosquito coils indoors generates smoke that can control mosquitoes effectively. This practice is currently used in numerous households in Asia, Africa, and South America. However, the smoke may contain pollutants of health concern. We conducted the present study to characterize the emissions from four common brands of mosquito coils from China and two common brands from Malaysia. We used mass balance equations to determine emission rates of fine particles (particulate matter < 2.5 microm in diameter; PM(2.5)), polycyclic aromatic hydrocarbons (PAHs), aldehydes, and ketones. Having applied these measured emission rates to predict indoor concentrations under realistic room conditions, we found that pollutant concentrations resulting from burning mosquito coils could substantially exceed health-based air quality standards or guidelines. Under the same combustion conditions, the tested Malaysian mosquito coils generated more measured pollutants than did the tested Chinese mosquito coils. We also identified a large suite of volatile organic compounds, including carcinogens and suspected carcinogens, in the coil smoke. In a set of experiments conducted in a room, we examined the size distribution of particulate matter contained in the coil smoke and found that the particles were ultrafine and fine. The findings from the present study suggest that exposure to the smoke of mosquito coils similar to the tested ones can pose significant acute and chronic health risks. For example, burning one mosquito coil would release the same amount of PM(2.5) mass as burning 75-137 cigarettes. The emission of formaldehyde from burning one coil can be as high as that released from burning 51 cigarettes.
  4. Andersen ZJ, Stafoggia M, Weinmayr G, Pedersen M, Galassi C, Jørgensen JT, et al.
    Environ Health Perspect, 2017 10 13;125(10):107005.
    PMID: 29033383 DOI: 10.1289/EHP1742
    BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent.

    OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women.

    METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

    RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2.5 {hazard ratio (HR)=1.08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3}, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3], PMcoarse[1.20 (95% CI: 0.96, 1.49 per 5 μg/m3], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p=0.04].

    CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. https://doi.org/10.1289/EHP1742.

  5. Lee S, Sbihi H, MacIsaac JL, Balshaw R, Ambalavanan A, Subbarao P, et al.
    Environ Health Perspect, 2024 Apr;132(4):47004.
    PMID: 38573328 DOI: 10.1289/EHP13034
    BACKGROUND: Evidence suggests that prenatal air pollution exposure alters DNA methylation (DNAm), which could go on to affect long-term health. It remains unclear whether DNAm alterations present at birth persist through early life. Identifying persistent DNAm changes would provide greater insight into the molecular mechanisms contributing to the association of prenatal air pollution exposure with atopic diseases.

    OBJECTIVES: This study investigated DNAm differences associated with prenatal nitrogen dioxide (NO2) exposure (a surrogate measure of traffic-related air pollution) at birth and 1 y of age and examined their role in atopic disease. We focused on regions showing persistent DNAm differences from birth to 1 y of age and regions uniquely associated with postnatal NO2 exposure.

    METHODS: Microarrays measured DNAm at birth and at 1 y of age for an atopy-enriched subset of Canadian Health Infant Longitudinal Development (CHILD) study participants. Individual and regional DNAm differences associated with prenatal NO2 (n=128) were identified, and their persistence at age 1 y were investigated using linear mixed effects models (n=124). Postnatal-specific DNAm differences (n=125) were isolated, and their association with NO2 in the first year of life was examined. Causal mediation investigated whether DNAm differences mediated associations between NO2 and age 1 y atopy or wheeze. Analyses were repeated using biological sex-stratified data.

    RESULTS: At birth (n=128), 18 regions of DNAm were associated with NO2, with several annotated to HOX genes. Some of these regions were specifically identified in males (n=73), but not females (n=55). The effect of prenatal NO2 across CpGs within altered regions persisted at 1 y of age. No significant mediation effects were identified. Sex-stratified analyses identified postnatal-specific DNAm alterations.

    DISCUSSION: Regional cord blood DNAm differences associated with prenatal NO2 persisted through at least the first year of life in CHILD participants. Some differences may represent sex-specific alterations, but replication in larger cohorts is needed. The early postnatal period remained a sensitive window to DNAm perturbations. https://doi.org/10.1289/EHP13034.

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