Children’s lung health improves with decreasing air pollution

Research, supported in part by NIEHS, shows that decreases in ambient air pollution in Southern California were associated with significant reductions in respiratory symptoms in children with and without asthma.

Since 1992, air pollution reduction policies and strategies have significantly improved air quality across Southern California. To find out how these improvements affected lung health, the researchers examined data from a total of 4,602 children in eight Southern California communities. They were all part of the Southern California Children’s Health Study over three time periods — from 1993 to 2001, 1996 to 2004, or 2003 to 2012. Researchers tracked bronchitic symptoms, including presence of a daily cough for three or more consecutive months, congestion or phlegm not related to a cold, and inflammation of the mucous membranes.

The authors report that decreases in ambient concentrations of nitrogen dioxide, ozone, and two sizes of particulate matter — less than 10 microns and less than 2.5 microns — were associated with significant decreases in bronchitic symptoms in children with and without asthma. Children with asthma showed proportionally larger symptom reductions, which remained persistent through age 15. Communities with the highest improvements in air quality exhibited the largest reductions in bronchitic symptoms.

Although the study does not provide a causal link between air pollution reduction and improved bronchitic symptoms, the findings support the potential benefit of air pollution reduction on asthma control.

Citation: Berhane K, Chang CC, McConnell R, Gauderman WJ, Avol E, Rapapport E, Urman R, Lurmann F, Gilliland F. 2016. Association of changes in air quality with bronchitic symptoms in children in California, 1993-2012. JAMA 315(14):1491-1501.

Pollutants found in fish inhibit natural defense system in people

NIEHS grantees report that environmental pollutants found in fish reduced the effectiveness of the human body’s natural system for expelling harmful contaminants. The new information gained from this study could help improve assessment of human health risks from eating contaminated seafood.

The researchers were interested in finding out how P-glycoprotein (P-gp), a transporter protein that expels foreign chemicals from the body, could rid cells of persistent organic pollutants found in seafood. Persistent organic pollutants are hazardous, man-made chemicals that persist in the environment and bioaccumulate in people and animals.

The scientists conducted a biochemical analysis to better understand how these proteins in humans and mice interact with persistent organic pollutants that are found most commonly in people, but are also detected in the muscle tissues of yellowfin tuna from the Gulf of Mexico. The pollutants included in the study were dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethylene (DDE), dichlorodiphenyldichloroethane (DDD), dieldrin, endrin, three forms of polychlorinated biphenyls, and two forms of polybrominated diphenyl ethers, including the common flame retardant PBDE-100.

The researchers found that all ten pollutants interfered with the ability of P-gp to clear toxicants from cells. The researchers also solved the structure of P-gp bound to PBDE-100, providing the first view of a pollutant binding to this transporter protein. This structural information may be used to design chemicals with better potential for elimination.

Citation: Nicklisch SC, Rees SD, McGrath AP, Gokirmak T, Bonito LT, Vermeer LM, Cregger C, Loewen G, Sandin S, Chang G, Hamdoun A. 2016. Global marine pollutants inhibit P-glycoprotein: environmental levels, inhibitory effects, and cocrystal structure. Sci Adv 2(4):e1600001.

Women live longer in areas with more green vegetation

NIEHS grantees report that women live longer in areas with more green vegetation. The new findings show that planting vegetation may improve health in multiple ways.

To study the relationship between greenness and mortality, the researchers used satellite imagery to examine greenness around the homes of 108,630 women, from across the nation, who participated in the long-term Nurses' Health Study. From 2000 to 2008, the researchers observed 8,604 deaths in study participants.

After adjusting for age and other mortality risk factors, women with the highest levels of vegetation near their homes had a 12 percent lower death rate compared to women with the lowest levels of vegetation near their homes. The biggest differences in death rates came from kidney disease, respiratory disease, and cancer. The researchers also showed that improved mental health and social engagement were the strongest factors in lowering mortality rates, while increased physical activity and reduced air pollution also contributed. When researchers compared women in the areas with highest greenness to women in the lowest, they found a 41 percent lower death rate for kidney disease, 34 percent lower death rate for respiratory disease, and 13 percent lower death rate for cancer in the greenest areas. The majority, 84 percent, of study participants lived in urban areas, but the impact of greenness on mortality was consistent in both urban and rural regions.

Citation: James P, Hart JE, Banay RF, Laden F. 2016. Exposure to greenness and mortality in a nationwide prospective cohort study of women. Environ Health Perspect; doi:10.1289/ehp.1510363 [Online 14 April 2016].

Tumor suppressor gene more likely to be defective in children with autism

New findings from the NIEHS-funded Childhood Autism Risk from Genes and Environment (CHARGE) study show that children with autism and their fathers have markers of molecular stress and damage in the cell’s nucleus and mitochondria. The markers are altered p53 gene copy ratios and increased mitochondrial (mt) DNA deletions. In the presence of an environmental stressor, p53 stops cell division to allow repair of damaged DNA. The research results suggest that DNA repair capacity and genome instability might play a role in autism.

The study included 66 children with autism and their parents, as well as 46 age-matched, typically developing, children and their parents, all of whom participated in the CHARGE study. The investigators examined the mtDNA copy number and deletions, and p53 gene copy ratios, in lymphocytes from children and both parents.

Higher p53 gene copy ratios and mtDNA deletions were more that twice as common in children with autism. Fathers of children with autism showed double the incidence of mtDNA deletions of age-matched fathers of typically developing children, suggesting a role for deficient DNA repair capacity not necessarily tied to paternal age.

The researchers said that the mtDNA deletions and altered p53 gene copy ratios seem to result from genetics in children with more severe autism, although gene-environment interactions seem to play a greater role in children with less severe symptoms.

Citation: Wong S, Napoli E, Krakowiak P, Tassone F, Hertz-Picciotto I, Giulivi C. 2016. Role of p53, mitochondrial DNA deletions, and paternal age in autism: a case-control study. Pediatrics 137(4):e20151888.