Catherine J. Karr

A cohort study of traffic-related air pollution impacts on birth outcomes.

Background Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts. Objectives We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics. Methods With linked administrative data, we identified 70,249 singleton births (1999–2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) μm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. Results Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07–1.49] and an 11% (95% CI, 1.01–1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00–1.04; IDW: OR = 1.05; 95% CI, 1.03–1.08 per 10-μg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance. Conclusion Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.

Effect of early life exposure to air pollution on development of childhood asthma

Background There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case–control study. Methods We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 3–4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM10 and PM2.5), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis. Results A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO2, PM10, SO2, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04–1.12) for a 10-μg/m3 increase of NO, 1.12 (1.07–1.17) for a 10-μg/m3 increase in NO2, and 1.10 (1.06–1.13) for a 100-μg/m3 increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.

Baby Care Products: Possible Sources of Infant Phthalate Exposure

OBJECTIVES. Phthalates are man-made chemicals found in personal care and other products. Recent studies suggest that some phthalates can alter human male reproductive development, but sources of infant exposure have not been well characterized. We investigated the relationship between phthalate metabolite concentrations in infant urine and maternal reported use of dermally applied infant care products. METHODS. We measured 9 phthalate metabolites in 163 infants who were born in 2000–2005. An infant was considered to have been exposed to any infant care product that the mother reported using on her infant within 24 hours of urine collection. Results of multiple linear regression analyses are reported as the ratio of metabolite concentrations (with 95% confidence intervals) in exposed and unexposed infants. We standardized concentrations by forming z scores and examined combined exposure to multiple metabolites. RESULTS. In most (81%) infants, ≥7 phthalate metabolites were above the limit of detection. Exposure to lotion was predictive of monoethyl phthalate and monomethyl phthalate concentrations, powder of monoisobutyl phthalate, and shampoo of monomethyl phthalate. Z scores increased with number of products used. Most associations were stronger in younger infants. CONCLUSIONS. Phthalate exposure is widespread and variable in infants. Infant exposure to lotion, powder, and shampoo were significantly associated with increased urinary concentrations of monoethyl phthalate, monomethyl phthalate, and monoisobutyl phthalate, and associations increased with the number of products used. This association was strongest in young infants, who may be more vulnerable to developmental and reproductive toxicity of phthalates given their immature metabolic system capability and increased dosage per unit body surface area.

Methodological issues in studies of air pollution and reproductive health

In the past decade there have been an increasing number of scientific studies describing possible effects of air pollution on perinatal health. These papers have mostly focused on commonly monitored air pollutants, primarily ozone (O(3)), particulate matter (PM), sulfur dioxide (SO(2)), carbon monoxide (CO), and nitrogen dioxide (NO(2)), and various indices of perinatal health, including fetal growth, pregnancy duration, and infant mortality. While most published studies have found some marker of air pollution related to some types of perinatal outcomes, variability exists in the nature of the pollutants and outcomes associated. Synthesis of the findings has been difficult for various reasons, including differences in study design and analysis. A workshop was held in September 2007 to discuss methodological differences in the published studies as a basis for understanding differences in study findings and to identify priorities for future research, including novel approaches for existing data. Four broad topic areas were considered: confounding and effect modification, spatial and temporal exposure variations, vulnerable windows of exposure, and multiple pollutants. Here we present a synopsis of the methodological issues and challenges in each area and make recommendations for future study. Two key recommendations include: (1) parallel analyses of existing data sets using a standardized methodological approach to disentangle true differences in associations from methodological differences among studies; and (2) identification of animal studies to inform important mechanistic research gaps. This work is of critical public health importance because of widespread exposure and because perinatal outcomes are important markers of future child and adult health.

Policy statement - Tobacco use: A pediatric disease

Tobacco use and secondhand tobacco-smoke (SHS) exposure are major national and international health concerns. Pediatricians and other clinicians who care for children are uniquely positioned to assist patients and families with tobacco-use prevention and treatment. Understanding the nature and extent of tobacco use and SHS exposure is an essential first step toward the goal of eliminating tobacco use and its consequences in the pediatric population. The next steps include counseling patients and family members to avoid SHS exposures or cease tobacco use; advocacy for policies that protect children from SHS exposure; and elimination of tobacco use in the media, public places, and homes. Three overarching principles of this policy can be identified: (1) there is no safe way to use tobacco; (2) there is no safe level or duration of exposure to SHS; and (3) the financial and political power of individuals, organizations, and government should be used to support tobacco control. Pediatricians are advised not to smoke or use tobacco; to make their homes, cars, and workplaces tobacco free; to consider tobacco control when making personal and professional decisions; to support and advocate for comprehensive tobacco control; and to advise parents and patients not to start using tobacco or to quit if they are already using tobacco. Prohibiting both tobacco advertising and the use of tobacco products in the media is recommended. Recommendations for eliminating SHS exposure and reducing tobacco use include attaining universal (1) smoke-free home, car, school, work, and play environments, both inside and outside, (2) treatment of tobacco use and dependence through employer, insurance, state, and federal supports, (3) implementation and enforcement of evidence-based tobacco-control measures in local, state, national, and international jurisdictions, and (4) financial and systems support for training in and research of effective ways to prevent and treat tobacco use and SHS exposure. Pediatricians, their staff and colleagues, and the American Academy of Pediatrics have key responsibilities in tobacco control to promote the health of children, adolescents, and young adults.

Pesticide exposure in children

Pesticides are a collective term for a wide array of chemicals intended to kill unwanted insects, plants, molds, and rodents. Food, water, and treatment in the home, yard, and school are all potential sources of children’s exposure. Exposures to pesticides may be overt or subacute, and effects range from acute to chronic toxicity. In 2008, pesticides were the ninth most common substance reported to poison control centers, and approximately 45% of all reports of pesticide poisoning were for children. Organophosphate and carbamate poisoning are perhaps the most widely known acute poisoning syndromes, can be diagnosed by depressed red blood cell cholinesterase levels, and have available antidotal therapy. However, numerous other pesticides that may cause acute toxicity, such as pyrethroid and neonicotinoid insecticides, herbicides, fungicides, and rodenticides, also have specific toxic effects; recognition of these effects may help identify acute exposures. Evidence is increasingly emerging about chronic health implications from both acute and chronic exposure. A growing body of epidemiological evidence demonstrates associations between parental use of pesticides, particularly insecticides, with acute lymphocytic leukemia and brain tumors. Prenatal, household, and occupational exposures (maternal and paternal) appear to be the largest risks. Prospective cohort studies link early-life exposure to organophosphates and organochlorine pesticides (primarily DDT) with adverse effects on neurodevelopment and behavior. Among the findings associated with increased pesticide levels are poorer mental development by using the Bayley index and increased scores on measures assessing pervasive developmental disorder, inattention, and attention-deficit/hyperactivity disorder. Related animal toxicology studies provide supportive biological plausibility for these findings. Additional data suggest that there may also be an association between parental pesticide use and adverse birth outcomes including physical birth defects, low birth weight, and fetal death, although the data are less robust than for cancer and neurodevelopmental effects. Children’s exposures to pesticides should be limited as much as possible.

Community Health Workers and Environmental Interventions for Children with Asthma: A Systematic Review

Community health worker (CHW)–delivered, home-based environmental interventions for pediatric asthma were systematically reviewed. Seven PubMed/MEDLINE listed randomized controlled trials that encompassed the following intervention criteria were identified: (1) home-based; (2) delivered by a CHW; (3) delivered to families with children with asthma; and (4) addressed multiple environmental triggers for asthma. Details of research design, intervention type, and setting, interventionist, population served, and the evaluated outcomes were abstracted. Outcome assessment was broad and non-uniform. Categories included direct mediators of improved health outcomes, such as trigger-related knowledge, trigger reduction behaviors and allergen or exposure levels, and asthma-related health outcomes: change in lung function, medication use, asthma symptoms, activity limitations, and health care utilization. Indirect mediators of health outcomes, or psychosocial influences on health, were measured in few studies. Overall, the studies consistently identified positive outcomes associated with CHW-delivered interventions, including decreased asthma symptoms, daytime activity limitations, and emergency and urgent care use. However, improvements in trigger reduction behaviors and allergen levels, hypothesized mediators of these outcomes, were inconsistent. Trigger reduction behaviors appeared to be tied to study-based resource provision. To better understand the mechanism through which CHW-led environmental interventions cause a change in asthma-related health outcomes, information on the theoretical concepts that mediate behavior change in trigger control (self-efficacy, social support) is needed. In addition, evaluating the influence of CHWs as clinic liaisons that enhance access to health professionals, complement clinic-based teaching, and improve appropriate use of asthma medications should be considered, alongside their effect on environmental management. A conceptual model identifying pathways for future investigation is presented.

Descriptive Epidemiological Features of Bronchiolitis in a Population-Based Cohort

OBJECTIVE. The goal was to investigate the epidemiological features of incident bronchiolitis by using a population-based infant cohort. METHODS. Outpatient and inpatient health records were used to identify incident bronchiolitis cases among 93 058 singleton infants born in the Georgia Air Basin between 1999 and 2002. Additional health-related databases were linked to provide data on sociodemographic variables, maternal characteristics, and birth outcome measures. RESULTS. From 1999 to 2002, bronchiolitis accounted for 12 474 incident health care encounters (inpatient or outpatient contacts) during the first year of life (134.2 cases per 1000 person-years). A total of 1588 hospitalized bronchiolitis cases were identified (17.1 cases per 1000 person-years). Adjusted Cox proportional-hazard analyses for both case definitions indicated an increased risk of incident bronchiolitis in the first year of life (follow-up period: 2–12 months) for boys, infants of First Nations status, infants with older siblings, and infants living in neighborhoods with smaller proportions of maternal postsecondary education. The risk also was elevated for infants born to young mothers (<20 years of age) or mothers who did not initiate breastfeeding in the hospital. Infants with low (1500–2400 g) or very low (<1500 g) birth weight and those with congenital anomalies also had increased risk. Maternal smoking during pregnancy increased the risk of hospitalized bronchiolitis. CONCLUSIONS. This population-based study of the epidemiological features of bronchiolitis provides evidence for intervening with high-risk infants and their families. Clinical and public health interventions are recommended for the modifiable risk factors of maternal breastfeeding and smoking and for modification of vulnerable environments where possible (eg, limiting exposure to other young children), during high-risk periods such as the first few months of life or the winter season.

Global climate change and children's health

There is a broad scientific consensus that the global climate is warming, the process is accelerating, and that human activities are very likely (>90% probability) the main cause. This warming will have effects on ecosystems and human health, many of them adverse. Children will experience both the direct and indirect effects of climate change. Actions taken by individuals, communities, businesses, and governments will affect the magnitude and rate of global climate change and resultant health impacts. This technical report reviews the nature of the global problem and anticipated health effects on children and supports the recommendations in the accompanying policy statement on climate change and childrens health.

Infant exposure to fine particulate matter and traffic and risk of hospitalization for RSV bronchiolitis in a region with lower ambient air pollution

Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM(2.5) and other metrics of traffic-derived air pollution exposure using a matched case-control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM(2.5) exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO(2) was applied to characterize subjects exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subjects residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mothers education, mothers smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (OR(adj)) and 95% confidence interval per 10 mcg/m(3) increase in lifetime PM(2.5) was 1.14, 0.88-1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (OR(adj) 1.17, 0.95-1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.