Associations between prenatal exposure to power plants and birth outcomes across the United States.

OBJECTIVES: Although there is growing evidence that in utero exposure to power plants increases the risk of adverse birth outcomes, studies have focused on coal-fired plants and single US locations, limiting generalizability. We used birth certificate data from 50 states and DC to examine the associations between prenatal exposure to power plants and birth outcomes overall and by race/ethnicity. METHODS: We linked 2009-2018 county-level microdata natality files on 34,674,911 singleton births from 50 states and DC with 9-month county-level averages of power plant fuel consumption based on month/year of birth. We estimated linear regression models for birth weight and gestational age and probit models for the dichotomous outcomes of low birth weight, small for gestational age (SGA), and preterm birth. We subsequently examined interactions between plant fuel consumption and race/ethnicity. RESULTS: Overall, 69.1% of counties had any power plant fuel consumption. Although we found no overall effects of prenatal exposure to power plants on birth weight or SGA, a significant interaction (both P < 0.01) revealed that a 10% increase in fuel consumption was associated with infants born to White women having slightly lower birth weights (1.76 g; 95% confidence interval = -2.87, -0.65) and higher risk of being born SGA (0.0002; 95% confidence interval = 0.0002, 0.0002). CONCLUSION: Power plants have negative effects on infant health, which exist independent of locality.

Dimensional structure and course of post-traumatic stress symptomatology in World Trade Center responders.

BACKGROUND: Post-traumatic stress disorder (PTSD) in response to the World Trade Center (WTC) disaster of 11 September 2001 (9/11) is one of the most prevalent and persistent health conditions among both professional (e.g. police) and non-traditional (e.g. construction worker) WTC responders, even several years after 9/11. However, little is known about the dimensionality and natural course of WTC-related PTSD symptomatology in these populations. METHOD: Data were analysed from 10 835 WTC responders, including 4035 police and 6800 non-traditional responders who were evaluated as part of the WTC Health Program, a clinic network in the New York area established by the National Institute for Occupational Safety and Health. Confirmatory factor analyses (CFAs) were used to evaluate structural models of PTSD symptom dimensionality; and autoregressive cross-lagged (ARCL) panel regressions were used to examine the prospective interrelationships among PTSD symptom clusters at 3, 6 and 8 years after 9/11. RESULTS: CFAs suggested that five stable symptom clusters best represent PTSD symptom dimensionality in both police and non-traditional WTC responders. This five-factor model was also invariant over time with respect to factor loadings and structural parameters, thereby demonstrating its longitudinal stability. ARCL panel regression analyses revealed that hyperarousal symptoms had a prominent role in predicting other symptom clusters of PTSD, with anxious arousal symptoms primarily driving re-experiencing symptoms, and dysphoric arousal symptoms primarily driving emotional numbing symptoms over time. CONCLUSIONS: Results of this study suggest that disaster-related PTSD symptomatology in WTC responders is best represented by five symptom dimensions. Anxious arousal symptoms, which are characterized by hypervigilance and exaggerated startle, may primarily drive re-experiencing symptoms, while dysphoric arousal symptoms, which are characterized by sleep disturbance, irritability/anger and concentration difficulties, may primarily drive emotional numbing symptoms over time. These results underscore the importance of assessment, monitoring and early intervention of hyperarousal symptoms in WTC and other disaster responders.

Trajectories of PTSD risk and resilience in World Trade Center responders: an 8-year prospective cohort study.

BACKGROUND: Longitudinal symptoms of post-traumatic stress disorder (PTSD) are often characterized by heterogeneous trajectories, which may have unique pre-, peri- and post-trauma risk and protective factors. To date, however, no study has evaluated the nature and determinants of predominant trajectories of PTSD symptoms in World Trade Center (WTC) responders. METHOD: A total of 10835 WTC responders, including 4035 professional police responders and 6800 non-traditional responders (e.g. construction workers) who participated in the WTC Health Program (WTC-HP), were evaluated an average of 3, 6 and 8 years after the WTC attacks. RESULTS: Among police responders, longitudinal PTSD symptoms were best characterized by four classes, with the majority (77.8%) in a resistant/resilient trajectory and the remainder exhibiting chronic (5.3%), recovering (8.4%) or delayed-onset (8.5%) symptom trajectories. Among non-traditional responders, a six-class solution was optimal, with fewer responders in a resistant/resilient trajectory (58.0%) and the remainder exhibiting recovering (12.3%), severe chronic (9.5%), subsyndromal increasing (7.3%), delayed-onset (6.7%) and moderate chronic (6.2%) trajectories. Prior psychiatric history, Hispanic ethnicity, severity of WTC exposure and WTC-related medical conditions were most strongly associated with symptomatic trajectories of PTSD symptoms in both groups of responders, whereas greater education and family and work support while working at the WTC site were protective against several of these trajectories. CONCLUSIONS: Trajectories of PTSD symptoms in WTC responders are heterogeneous and associated uniquely with pre-, peri- and post-trauma risk and protective factors. Police responders were more likely than non-traditional responders to exhibit a resistant/resilient trajectory. These results underscore the importance of prevention, screening and treatment efforts that target high-risk disaster responders, particularly those with prior psychiatric history, high levels of trauma exposure and work-related medical morbidities.

The World Trade Center health surveillance program: results of the first 10 years and implications for prevention.

BACKGROUND: The terrorist attacks on the World Trade Center (WTC) of September 11, 2001 resulted in the deaths of 2,823 persons. They also generated a long-lasting burden of multiple physical and mental health illnesses among the cohort of 50,000 rescue workers who responded to the attacks and in the 400,000 residents and workers in nearby areas of New York City. A comprehensive health surveillance program was developed from the first months after the accidents and was further developed in the subsequent ears. Individual exposure and health data were stored in ad hoc databases and produced epidemiological outcomes on the various exposure-related illnesses. METHODS: About 10 years of longitudinal assessment of this large cohort of WTC rescue and recovery workers, yielded data from participants in the WTC Screening, Monitoring, and Treatment Program. Police officers, firefighters, construction workers, and municipal workers were included in the cohort. Cumulative and annual incidence were estimated for various physical disorders including asthma, sinusitis, and gastroesophageal reflux disease, mental health disorders including depression, post-traumatic stress disorder [PTSD], and panic disorder. Respiratory functionality was also assessed. Exposure was characterized with qualitative parameter including working on the pile and being engulfed in the dust cloud, and quantitative parameters including the time of arrival on site and the exposure duration. RESULTS: Upper and lower respiratory conditions such as rhinosinusitis and asthma have been found in a significant number of people in WTC-exposed populations. A lack of appropriate respiratory protection may have contributed to these effects. Other commonly observed physical health conditions include gastro-esophageal reflux disease, obstructive sleep apnea and musculo-skeletal injuries. Many WTC-exposed individuals also suffer from mental health conditions, primarily post-traumatic stress disorder, depression, panic disorder, and substantial stress reaction. Recent studies suggest that WTC exposure may increase the risk of cancer and of mortality from cardiac disease. CONCLUSION: Ten years of systematic health surveillance after the 9/11 WTC attacks, show long lasting burden of physical and mental health problems. Continued monitoring and treatment of this population is needed for early diagnoses of initial clinical conditions that can be treated more effectively. The experience of September 11 offers also indications on how to approach the acute and delayed health effects of civilian catastrophes. Critical lessons are derived about the importance of having trained responders--medical and non-medical--in place in advance of disasters, and about the need to proceed with adequate exposure assessment in a timely manner.

Developmental neurotoxicity of industrial chemicals.

Neurodevelopmental disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common, costly, and can cause lifelong disability. Their causes are mostly unknown. A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function. Recognition of these risks has led to evidence-based programmes of prevention, such as elimination of lead additives in petrol. Although these prevention campaigns are highly successful, most were initiated only after substantial delays. Another 200 chemicals are known to cause clinical neurotoxic effects in adults. Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation. New, precautionary approaches that recognise the unique vulnerability of the developing brain are needed for testing and control of chemicals.

Abdominal diameter index: a more powerful anthropometric measure for prevalent coronary heart disease risk in adult males.

AIM: The authors wished to compare the strength of association of several anthropometric measures of body size and fat distribution among themselves and in comparison with other known risk factors for prevalent coronary heart disease (CHD). METHODS: Prevalent CHD was assessed in 466 middle-aged, male, multiracial Triborough Bridge and Tunnel Authority officers in New York City by verified history, electrocardiogram or exercise stress test. Anthropometric measures included body mass index, waist, hip and thigh circumferences, waist-hip ratio, waist-thigh ratio, sagittal abdominal diameter and abdominal diameter index (sagittal abdominal diameter/thigh circumference). Results were compared with other CHD risk factors measured simultaneously (history of diabetes, smoking, blood pressure, lipid profile, apolipoproteins A and B, lipoprotein (a), homocysteine, fibrinogen, urinary microalbumin, serum vitamin E and ferritin) and a calculated 10-year CHD risk using a Framingham algorithm (10-year Framingham CHD risk). RESULTS: CHD was found in 29 individuals. Of the six anthropometric measures, abdominal diameter index gave the largest and most significant standardized odds ratio (OR) for CHD [1.80, 95% confidence interval (CI) 1.20, 2.71], equivalent to 10-year Framingham CHD risk. Men in the highest compared with the lowest tertile of abdominal diameter index had a univariate OR of 5.47 (95% CI 1.55, 19.28) which was the only anthropometric measure that remained significant after adjusting for 10-year Framingham CHD risk. CONCLUSIONS: For middle-aged American men, abdominal diameter index may be the most powerful anthropometric measure of risk for prevalent CHD.

Children's environmental health. Lessons from the past and prospects for the future.

Environmental pediatrics is an area of pediatric medicine that has come a long way in the past 50 years. It has risen to importance in parallel with two developments: (1) the conquest in the industrialized nations of the major infectious diseases and their replacement by chronic conditions, such as asthma, cancer, developmental disabilities, and birth defects as the primary causes of illness and death in children and (2) the growing recognition that chemicals in the environment are responsible, at least in part, for these changes in patterns of disease. The challenge now to environmental pediatrics is to better understand the impact of chemical substances on the patterns of health and disease in children and to design evidence-based approaches to the treatment and prevention of childhood disease of environmental origin.

The rationale for a national prospective cohort study of environmental exposure and childhood development.

Evidence is growing that pre- and perinatal exposures and factors play a role in not only childhood but adulthood disorders. Therefore, there is a compelling need to undertake a national cohort study to evaluate the effects of such factors, ideally through adult life. Several recent developments, including advancements in computer technology, the management, storage, and analysis of biological specimens, and the rapid growth of genetic markers, facilitate the evaluation of the influence of environmental exposures on the subsequent risk of developmental abnormalities and disease. The rationale behind the establishment of such a cohort is discussed.

Exposure to hazardous substances and male reproductive health: a research framework.

The discovery in the mid-1970s that occupational exposures to pesticides could diminish or destroy the fertility of workers sparked concern about the effects of hazardous substances on male reproductive health. More recently, there is evidence that sperm quantity and quality may have declined worldwide, that the incidence of testicular cancer has progressively increased in many countries, and that other disorders of the male reproductive tract such as hypospadias and cryptorchidism may have also increased. There is growing concern that occupational factors and environmental chemical exposures, including in utero and childhood exposures to compounds with estrogenic activity, may be correlated with these observed changes in male reproductive health and fertility. We review the evidence and methodologies that have contributed to our current understanding of environmental effects on male reproductive health and fertility and discuss the methodologic issues which confront investigators in this area. One of the greatest challenges confronting researchers in this area is assessing and comparing results from existing studies. We elaborate recommendations for future research. Researchers in the field of male reproductive health should continue working to prioritize hazardous substances; elucidate the magnitude of male reproductive health effects, particularly in the areas of testicular cancer, hypospadias, and cryptorchidism; develop biomarkers of exposure to reproductive toxins and of reproductive health effects for research and clinical use; foster collaborative interdisciplinary research; and recognize the importance of standardized laboratory methods and sample archiving.

Occupational coronary heart disease among bridge and tunnel officers.

Traffic-control officers employed in New York City tunnels prior to 1981 have been at increased risk of mortality from coronary heart disease. In this study, the authors assessed current coronary heart disease prevalence and evaluated associations between coronary heart disease and occupational factors among New York City bridge and tunnel officers. A clinical cardiovascular disease surveillance and cross-sectional occupational epidemiologic study was conducted. The authors used comprehensive evaluations to identify current and prior incidences of coronary heart disease. Occupational risk factors evaluated included job strain, current and historic exposure to carbon monoxide, and occupational physical inactivity. Current carbon monoxide exposure was assessed via workshift changes in carboxyhemoglobin. Coronary heart disease occurred in 29 (5.5%) of the 526 bridge and tunnel officers examined. Risk of coronary heart disease was associated positively with total years each bridge and tunnel officer work had worked in that capacity (odds ratio = 1.64 for each decade of employment, adjusted for nonoccupational coronary heart disease risk factors). Carboxyhemoglobin levels were low in the subjects, and job strain and physical inactivity were very prevalent. Occupational factors contributed to the risk of coronary heart disease in New York City bridge and tunnel officers. The authors were unable to identify the specific factors that led to the increase in risk described.

The developing brain and the environment: an introduction.

mental retardation: timing and thresholds; (italic)b(/italic)) endocrine dysfunction and developmental disabilities: dose and target implications; (italic)c(/italic)) attention-deficit disorder-ADHD and learning disabilities; and (italic)d(/italic)) new horizons: extending the boundaries. Support for the Rochester conference came from both public and private sources. The National Institute of Environmental Health Sciences (NIEHS), the National Institute of Child Health and Human Development, and the EPA represented the federal government. The conference also received grants from several foundations: the Jennifer Altman Foundation, the Heinz Family Foundation, the National Alliance for Autism Research, the Violence Research Foundation, the Wacker Foundation, and the Winslow Foundation. The second of these conferences helped launch a new Center for Children's Health and the Environment at the Mount Sinai School of Medicine. It was held in New York City on 24-25 May 1999, and was convened specifically to consider the intersection between neurodevelopmental impairment, environmental chemicals, and prevention. Over 300 health scientists, pediatricians, and public health professionals examined the growing body of evidence linking environmental toxins to neurobehavioral disorders. The conference title was Environmental Influences on Children: Brain, Development, and Behavior. The conference began by reviewing well-known examples of deleterious effects of environmental chemicals, including lead and PCBs, on children's brains. The conferees then considered the potential impact of environmental chemicals on neurological disorders with particular focus on ADHD, autism, and Parkinson's disease. The inclusion of Parkinson's disease was intended to signal the notion that exposures in early life may have an influence on the evolution of neurological disease in later life. Support for the Mount Sinai conference came from the Superfund Basic Research Program (NIEHS); The Pew Charitable Trusts; the Institute for Health and the Environment at the University of Albany School of Public Health; the Agency for Toxic Substances and Disease Research (ATSDR); the Ambulatory Pediatric Association; Myron A. Mehlman, PhD; the National Center for Environmental Assessment (EPA); the National Center for Environmental Health (CDC); the National Institute of Child Health and Human Development; the Office of Children's Health Protection (EPA); Physicians for Social Responsibility; The New York Academy of Medicine; The New York Community Trust; and the Wallace Genetic Foundation. The impact of environmental toxins on children's health has become a topic of major concern in the federal government. Eight new research centers in children's environmental health have been established in the past 2 years with joint funding from EPA and NIEHS. Clinical units that specialize in the treatment of children with environmentally induced illness have been developed across the nation with grant support from ATSDR. The American Academy of Pediatrics has just published its (italic)Handbook of Pediatric Environmental Health (/italic)((italic)17(/italic)), the "Green Book," which is available to pediatricians throughout the Americas. Children's environmental health has climbed to a critical position as we launch the new millennium. This monograph marks a significant milestone in the evolution of this emerging discipline.

A cluster of pediatric metallic mercury exposure cases treated with meso-2,3-dimercaptosuccinic acid (DMSA)

Nine children and their mother were exposed to vapors of metallic mercury. The source of the exposure appears to have been a 6-oz vial of mercury taken from a neighbor's home. The neighbor reportedly operated a business preparing mercury-filled amulets for practitioners of the Afro-Caribbean religion Santeria. At diagnosis, urinary mercury levels in the children ranged from 61 to 1,213 microg/g creatinine, with a geometric mean of 214.3 microg/m creatinine. All of the children were asymptomatic. To prevent development of neurotoxicity, we treated the children with oral meso-2,3-dimercaptosuccinic acid (DMSA). During chelation, the geometric mean urine level rose initially by 268% to 573.2 microg mercury/g creatinine (p<0.0005). At the 6-week follow-up examination after treatment, the geometric mean urine mercury level had fallen to 102.1 microg/g creatinine, which was 17.8% of the geometric mean level observed during treatment (p<0.0005) and 47.6% of the original baseline level (p<0.001). Thus, oral chelation with DMSA produced a significant mercury diuresis in these children. We observed no adverse side effects of treatment. DMSA appears to be an effective and safe chelating agent for treatment of pediatric overexposure to metallic mercury.

Work-related death: a continuing epidemic.

Worldwide, work-related illnesses and injuries kill approximately 1.1 million people per year. In 1992, an estimated 65,000 people in the United States died of occupational injuries or illness. Most estimates indicate that occupational diseases account for far more fatalities than occupational injuries. However, an accurate enumeration of occupational disease fatalities is hampered by a paucity of data, owing to underdiagnosis of occupational diseases and inadequacy of current surveillance systems. In this commentary, the authors review the epidemiology of death due to occupational disease and injury in the United States and discuss vulnerable populations, emerging trends, and prevention strategies for this ongoing public health problem.