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1.
Environ Epidemiol ; 4(4): e0102, 2020 Aug.
Article in English | MEDLINE | ID: mdl-32832841

ABSTRACT

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are a class of ubiquitous, environmental chemicals that may have endocrine disrupting capabilities. We investigated whether childhood exposure to PAHs was associated with adiposity and pubertal timing in a longitudinal study of 404 girls enrolled in the Northern California site of the Breast Cancer and the Environment Research Program cohort. METHODS: Baseline urinary samples from girls aged 6-8-years-old were assayed for 2-naphthol, fluorene metabolites, phenanthrene metabolites, 1-hydroxypyrene, and sum of PAH metabolites. Mixed-effects linear models were used to estimate how concentrations of PAH metabolites were related to changes in girl's body mass index (BMI) and waist-to-height ratio from age 7 through 16 years old. Accelerated failure time models were used to estimate age of pubertal onset (Tanner stages 2 or higher for breast and pubic hair development). RESULTS: Higher adiposity measurements among high tertiles of baseline PAH metabolites were evident at age 7 years old and increased thereafter (i.e., BMI for all PAH metabolites, waist-to-height ratio for fluorene and phenanthrene metabolites) or leveled off (i.e., waist-to-height ratio for 2-naphthol, 1-hydroxypyrene, sum of PAHs). Among girls overweight/obese at baseline, median age of breast development onset for high tertiles was 9.1-9.4 years old compared with 10-10.2 years old for low tertiles for all PAH metabolites; in contrast, found no association or slightly later onset of breast development for girls with normal weight at baseline. DISCUSSION: These results suggest that exposure to specific PAHs during childhood may influence adiposity throughout adolescence and effect pubertal timing.

2.
Article in English | MEDLINE | ID: mdl-31671594

ABSTRACT

Childhood environmental tobacco smoke (ETS) exposure is a risk factor for adverse health outcomes and may disproportionately burden lower socioeconomic status groups, exacerbating health disparities. We explored associations of demographic factors, stressful life events, and chemical co-exposures, with cotinine levels, among girls in the CYGNET Study. Data were collected from families of girls aged 6-8 years old in Northern California, through clinic exams, questionnaires and biospecimens (n = 421). Linear regression and factor analysis were conducted to explore predictors of urinary cotinine and co-exposure body burdens, respectively. In unadjusted models, geometric mean cotinine concentrations were higher among Black (0.59 ug/g creatinine) than non-Hispanic white (0.27), Asian (0.32), or Hispanic (0.34) participants. Following adjustment, living in a rented home, lower primary caregiver education, and lack of two biologic parents in the home were associated with higher cotinine concentrations. Girls who experienced parental separation or unemployment in the family had higher unadjusted cotinine concentrations. Higher cotinine was also associated with higher polybrominated diphenyl ether and metals concentrations. Our findings have environmental justice implications as Black and socio-economically disadvantaged young girls experienced higher ETS exposure, also associated with higher exposure to other chemicals. Efforts to reduce ETS and co-exposures should account for other disparity-related factors.


Subject(s)
Family Characteristics , Stress, Psychological/epidemiology , Tobacco Smoke Pollution/analysis , Adult , California/epidemiology , Caregivers , Child , Cotinine/blood , Environmental Exposure/analysis , Factor Analysis, Statistical , Female , Halogenated Diphenyl Ethers/analysis , Health Status Disparities , Humans , Linear Models , Metals/analysis , Racial Groups/statistics & numerical data , Social Class , Socioeconomic Factors , Surveys and Questionnaires
3.
Environ Res ; 171: 581-592, 2019 04.
Article in English | MEDLINE | ID: mdl-30448205

ABSTRACT

In 2011 the International Agency for Research on Cancer classified radiofrequency electromagnetic fields (RF EMF) from cell phones as possibly carcinogenic to humans. The National Toxicology Program and the Ramazzini Institute have both reported that RF EMF exposures significantly increase gliomas and Schwannomas of the heart in rodent studies. Recent studies indicate that RF EMF exposures from cell phones have negative impacts on animal cells and cognitive and/or behavioral development in children. Case-control epidemiological studies have found evidence for cell phone use and increased risk for glioma and localization of the glioma associated with the consistent exposure site of regular cell phone use. Understanding the exposure level, or power density, from RF EMF emitted by cell phones under real-world usage and signal reception conditions, as distinct from the published measurements of maximum Specific Absorption Rate values, may help cell phone users decide whether to take behavioral steps to reduce RF EMF exposure. Exposure measurements were conducted on phone models from four major mobile network operators (MNOs) in the USA for calls received under strong and weak reception signal conditions, near the phone face and at several distances up to 48 cm. RF EMF exposure from all phones was found to be greater under weak (1-2 display bars) than under strong (4-5 display bars) reception signal conditions by up to four orders of magnitude. Notably, RF EMF exposure levels under weak reception signal conditions at a distance of 48 cm from the phone were similar to or greater than those detected under strong reception signal conditions at a distance of 4 cm. Under weak reception signal conditions, power density reductions of up to 90% occurred at 16 cm typical for speaker phone or texting over the 4 cm near-ear exposure. The results of this investigation of second-generation (2G) technology suggest that reduced and precautionary use of cell phones under weak signal conditions could lower a user's RF EMF exposure by up to several orders of magnitude. Bluetooth headset power density exposures were 10-400 times lower than those of the cell phones to which they were connected and dependent on the headset rather than the connected phone. The results of this study informed the development of public health guidance regarding cell phone use.


Subject(s)
Cell Phone , Electromagnetic Fields , Environmental Exposure , Case-Control Studies , Child , Humans , Radio Waves
4.
Environ Res ; 165: 46-54, 2018 08.
Article in English | MEDLINE | ID: mdl-29665464

ABSTRACT

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs), a class of chemicals produced as combustion by-products, have been associated with endocrine disruption. To understand exposure in children, who have been less studied than adults, we examined PAH metabolite concentrations by demographic characteristics, potential sources of exposure, and variability over time, in a cohort study of pre- and peri-pubertal girls in Northern California. METHODS: Urinary concentrations of ten PAH metabolites and cotinine were quantified in 431 girls age 6-8 years at baseline. Characteristics obtained from parental interview, physical exam, and linked traffic data were examined as predictors of PAH metabolite concentrations using multivariable linear regression. A subset of girls (n = 100) had repeat measures of PAH metabolites in the second and fourth years of the study. We calculated the intraclass correlation coefficient (ICC), Spearman correlation coefficients, and how well the quartile ranking by a single measurement represented the four-year average PAH biomarker concentration. RESULTS: Eight PAH metabolites were detected in ≥ 95% of the girls. The most consistent predictors of PAH biomarker concentrations were cotinine concentration, grilled food consumption, and region of residence, with some variation by demographics and season. After adjustment, select PAH metabolite concentrations were higher for Hispanic and Asian girls, and lower among black girls; 2-naphthol concentrations were higher in girls from lower income households. Other than 1-naphthol, there was modest reproducibility over time (ICCs between 0.18 and 0.49) and the concentration from a single spot sample was able to reliably rank exposure into quartiles consistent with the multi-year average. CONCLUSIONS: These results confirm diet and environmental tobacco smoke exposure as the main sources of PAHs. Controlling for these sources, differences in concentrations still existed by race for specific PAH metabolites and by income for 2-naphthol. The modest temporal variability implies adequate exposure assignment using concentrations from a single sample to define a multi-year exposure timeframe for epidemiologic exposure-response studies.


Subject(s)
Biomarkers , Environmental Exposure , Environmental Pollutants , Polycyclic Aromatic Hydrocarbons , Adolescent , Biomarkers/urine , California , Child , Cohort Studies , Environmental Exposure/statistics & numerical data , Environmental Pollutants/urine , Female , Humans , Polycyclic Aromatic Hydrocarbons/urine , Race Factors , Reproducibility of Results , Time Factors
5.
Epidemiology ; 28(5): 719-727, 2017 09.
Article in English | MEDLINE | ID: mdl-28661938

ABSTRACT

BACKGROUND: Tobacco smoke contains known hormonally active chemicals and reproductive toxicants. Several studies have examined prenatal maternal smoking and offspring age at menarche, but few examined earlier pubertal markers, nor accounted for exposure during childhood. Our objective was to examine pre- and postnatal smoke exposure in relation to timing of early pubertal events. METHODS: An ethnically diverse cohort of 1239 girls was enrolled at age 6-8 years old for a longitudinal study of puberty at three US sites. Girls participated in annual or semi-annual exams to measure anthropometry and Tanner breast and pubic hair stages. Prenatal and current tobacco smoke exposures, as well as covariates, were obtained from parent questionnaire. Cotinine was measured in urine collected at enrollment. Using accelerated failure time models, we calculated adjusted time ratios for age at pubertal onset (maturation stages 2 or higher) and smoke exposure. RESULTS: Girls with higher prenatal (≥5 cigarettes per day) or secondhand smoke exposure had earlier pubic hair development than unexposed (adjusted time ratio: 0.92 [95% CI = 0.87, 0.97] and 0.94 [95% CI = 0.90, 0.97], respectively). Including both exposures in the same model yielded similar associations. Higher urinary cotinine quartiles were associated with younger age at breast and pubic hair onset in unadjusted models, but not after adjustment. CONCLUSIONS: Greater prenatal and childhood secondhand smoke exposure were associated with earlier onset of pubic hair, but not breast, development. These exposures represent modifiable risk factors for early pubertal development that should be considered for addition to the extensive list of adverse effects from tobacco smoke.


Subject(s)
Menarche/drug effects , Tobacco Smoke Pollution/adverse effects , Age Factors , Child , Cotinine/urine , Female , Humans , Longitudinal Studies , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Tobacco Smoke Pollution/analysis
6.
Environ Sci Technol ; 50(22): 12464-12472, 2016 11 15.
Article in English | MEDLINE | ID: mdl-27700069

ABSTRACT

Exposures to environmental pollutants in utero may increase the risk of adverse health effects. We measured the concentrations of 59 potentially harmful chemicals in 77 maternal and 65 paired umbilical cord blood samples collected in San Francisco during 2010-2011, including polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), polybrominated diphenyl ethers (PBDEs), hydroxylated PBDEs (OH-PBDEs), and perfluorinated compounds (PFCs) in serum and metals in whole blood. Consistent with previous studies, we found evidence that concentrations of mercury (Hg) and lower-brominated PBDEs were often higher in umbilical cord blood or serum than in maternal samples (median cord:maternal ratio > 1), while for most PFCs and lead (Pb), concentrations in cord blood or serum were generally equal to or lower than their maternal pair (median cord:maternal ratio ≤ 1). In contrast to the conclusions of a recent review, we found evidence that several PCBs and OCPs were also often higher in cord than maternal serum (median cord:maternal ratio > 1) when concentrations are assessed on a lipid-adjusted basis. Our findings suggest that for many chemicals, fetuses may experience higher exposures than their mothers and highlight the need to characterize potential health risks and inform policies aimed at reducing sources of exposure.


Subject(s)
Environmental Pollutants , Halogenated Diphenyl Ethers , Maternal Exposure , Environmental Monitoring , Female , Humans , Hydrocarbons, Chlorinated , Infant, Newborn , Maternal-Fetal Exchange , Polychlorinated Biphenyls , Pregnancy , San Francisco , Urban Population
7.
Article in English | MEDLINE | ID: mdl-27005646

ABSTRACT

Mortality increases during periods of elevated heat. Identification of vulnerable subgroups by demographics, causes of death, and geographic regions, including deaths occurring at home, is needed to inform public health prevention efforts. We calculated mortality relative risks (RRs) and excess deaths associated with a large-scale California heat wave in 2006, comparing deaths during the heat wave with reference days. For total (all-place) and at-home mortality, we examined risks by demographic factors, internal and external causes of death, and building climate zones. During the heat wave, 582 excess deaths occurred, a 5% increase over expected (RR = 1.05, 95% confidence interval (CI) 1.03-1.08). Sixty-six percent of excess deaths were at home (RR = 1.12, CI 1.07-1.16). Total mortality risk was higher among those aged 35-44 years than ≥ 65, and among Hispanics than whites. Deaths from external causes increased more sharply (RR = 1.18, CI 1.10-1.27) than from internal causes (RR = 1.04, CI 1.02-1.07). Geographically, risk varied by building climate zone; the highest risks of at-home death occurred in the northernmost coastal zone (RR = 1.58, CI 1.01-2.48) and the southernmost zone of California's Central Valley (RR = 1.43, CI 1.21-1.68). Heat wave mortality risk varied across subpopulations, and some patterns of vulnerability differed from those previously identified. Public health efforts should also address at-home mortality, non-elderly adults, external causes, and at-risk geographic regions.


Subject(s)
Cause of Death , Heat Stress Disorders/etiology , Heat Stress Disorders/mortality , Hispanic or Latino/statistics & numerical data , Hot Temperature/adverse effects , Adolescent , Adult , Aged , Aged, 80 and over , California/epidemiology , Child , Child, Preschool , Data Interpretation, Statistical , Environment Design , Female , Heat Stress Disorders/epidemiology , Humans , Infant , Infant, Newborn , Male , Middle Aged , Risk Assessment , Socioeconomic Factors , Young Adult
8.
J Occup Environ Med ; 57(1): 88-97, 2015 Jan.
Article in English | MEDLINE | ID: mdl-25563545

ABSTRACT

OBJECTIVE: To assess California firefighters' blood concentrations of selected chemicals and compare with a representative US population. METHODS: We report laboratory methods and analytic results for cadmium, lead, mercury, and manganese in whole blood and 12 serum perfluorinated chemicals in a sample of 101 Southern California firefighters. RESULTS: Firefighters' blood metal concentrations were all similar to or lower than the National Health and Nutrition Examination Survey (NHANES) values, except for six participants whose mercury concentrations (range: 9.79 to 13.42 µg/L) were close to or higher than the NHANES reporting threshold of 10 µg/L. Perfluorodecanoic acid concentrations were elevated compared with NHANES and other firefighter studies. CONCLUSIONS: Perfluorodecanoic acid concentrations were three times higher in this firefighter group than in NHANES adult males. Firefighters may have unidentified sources of occupational exposure to perfluorinated chemicals.


Subject(s)
Environmental Monitoring/methods , Firefighters , Fires , Occupational Exposure/analysis , Adult , Age Factors , Alkanesulfonic Acids/blood , Cadmium/blood , California , Decanoic Acids/blood , Fatty Acids , Female , Fluorocarbons/blood , Heptanoic Acids/blood , Humans , Hydrocarbons, Fluorinated/blood , Lead/blood , Male , Manganese/blood , Mercury/blood , Middle Aged , Nutrition Surveys , Occupational Exposure/standards , Sulfonamides/blood , Young Adult
9.
Am J Obstet Gynecol ; 209(2): e4-5, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23685000

ABSTRACT

Mercury exposure during pregnancy can have serious health effects for a developing fetus including impacting the child's neurologic and cognitive development. Through biomonitoring in a low-income Latina population in California, we identified a patient with high levels of mercury and traced the source to face creams purchased in a pharmacy in Mexico.


Subject(s)
Environmental Monitoring , Mercury/blood , Skin Cream/chemistry , Female , Fetus/drug effects , Humans , Mexico , Pregnancy
10.
J Occup Environ Med ; 54(5): 564-71, 2012 May.
Article in English | MEDLINE | ID: mdl-22504958

ABSTRACT

OBJECTIVE: To describe the investigation of a 2007 occupational coccidioidomycosis outbreak in California, recommend prevention measures, and assess statewide disease burden. METHODS: We evaluated the worksite, observed work practices, interviewed the workers and employer, reviewed medical records, provided prevention recommendations including risk-based respirator selection, and analyzed statewide workers' compensation claims. RESULTS: Ten of 12 workers developed acute pulmonary coccidioidomycosis; none used respiratory protection. We recommended engineering, work practice, and administrative controls, powered air-purifying respirator use, and medical care. Occupational coccidioidomycosis incidence nearly quadrupled in California from 2000 to 2006, with the highest rates in construction and agricultural workers. CONCLUSIONS: Construction workers are at risk for occupational coccidioidomycosis. The high attack rate in this outbreak was due to lack of awareness, rainfall patterns, soil disruption, and failure to use appropriate controls. Multiple risk-based measures are needed to control occupational coccidioidomycosis in endemic areas.


Subject(s)
Coccidioides , Coccidioidomycosis/epidemiology , Disease Outbreaks , Inhalation Exposure/prevention & control , Occupational Diseases/epidemiology , Population Surveillance , Soil Microbiology , California/epidemiology , Coccidioidomycosis/prevention & control , Construction Industry/organization & administration , Health Knowledge, Attitudes, Practice , Humans , Occupational Diseases/prevention & control , Organizational Policy , Respiratory Protective Devices , Workers' Compensation/statistics & numerical data
11.
Rev Environ Health ; 25(4): 261-305, 2010.
Article in English | MEDLINE | ID: mdl-21268442

ABSTRACT

Since the 1970s, an increasing number of regulations have expanded the use of brominated and chlorinated flame retardants. Many of these chemicals are now recognized as global contaminants and are associated with adverse health effects in animals and humans, including endocrine and thyroid disruption, immunotoxicity, reproductive toxicity, cancer, and adverse effects on fetal and child development and neurologic function. Some flame retardants such as polybrominated diphenyl ethers (PBDEs) have been banned or voluntarily phased out by manufacturers because of their environmental persistence and toxicity, only to be replaced by other organohalogens of unknown toxicity. Despite restrictions on further production in some countries, consumer products previously treated with banned retardants are still in use and continue to release toxic chemicals into the environment, and the worldwide use of organohalogen retardants continues to increase. This paper examines major uses and known toxic effects of commonly-used organohalogen flame retardants, replacements for those that have been phased out, their combustion by-products, and their effectiveness at reducing fire hazard. Policy and other solutions to maintain fire safety while reducing toxicity are suggested. The major conclusions are: (1) Flammability regulations can cause greater adverse environmental and health impacts than fire safety benefits. (2) The current options for end-of-life disposal of products treated with organohalogens retardants are problematic. (3) Life-cycle analyses evaluating benefits and risks should consider the health and environmental effects of the chemicals, as well as their fire safety impacts. (4) Most fire deaths and most fire injuries result from inhaling carbon monoxide, irritant gases, and soot. The incorporation of organohalogens can increase the yield of these toxic by-products during combustion. (5) Fire-safe cigarettes, fire-safe candles, child-resistant lighters, sprinklers, and smoke detectors can prevent fires without the potential adverse effects of flame retardant chemicals. (6) Alternatives to organohalogen flame retardant chemicals include using less flammable materials, design changes, and safer chemicals. To date, before evaluating their health and environmental impacts, many flame retardant chemicals have been produced and used, resulting in high levels of human exposure. As a growing literature continues to find adverse impacts from such chemicals, a more systematic approach to their regulation is needed. Before implementing new flammability standards, decision-makers should evaluate the potential fire safety benefit versus the health and environmental impacts of the chemicals, materials, or technologies likely to be used to meet the standard. Reducing the use of toxic or untested flame retardant chemicals in consumer products can protect human and animal health and the global environment without compromising fire safety.


Subject(s)
Environmental Pollutants/toxicity , Environmental Pollution/adverse effects , Fires/prevention & control , Flame Retardants/toxicity , Hydrocarbons, Halogenated/toxicity , Animals , Environmental Pollution/legislation & jurisprudence , Humans , Policy , Refuse Disposal
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