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P J Landrigan

Publications and source records attributed to P J Landrigan.

At least 19 recordsLinked to original sources
PubMed2006

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.

Adolescent↗
PubMed2005

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.

Abdomen↗
PubMed2001

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.

Adolescent↗
PubMed2001

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.

Child↗
PubMed2000

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.

Administration, Oral↗
PubMed2000

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.

Biomarkers↗
PubMed2000

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.

Brain↗
PubMed2000

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.

Accidents, Occupational↗
PubMed1999

Risk assessment for children and other sensitive populations.

Children form a unique subgroup within the population who require special consideration in risk assessment. Children are not little adults. Their tissues and organs grow rapidly, developing and differentiating. These development processes create windows of great vulnerability to environmental toxicants. Furthermore, the exposure patterns of children to environmental chemicals are very different from those of adults. Traditional risk assessment has generally failed to consider the special exposures and the unique susceptibilities of infants and children. Adoption of a new child-centered agenda for research and risk assessment is necessary if disease in children of toxic environmental origin is to be identified, understood, controlled, and prevented. This agenda needs to be multidisciplinary. Specific requirements within the agenda include: (1) exploration and quantification of unique patterns of exposure for children; (2) adoption of new, more sensitive approaches to testing chemicals that can recognize the consequences of exposure during early development; (3) identification, through clinical and epidemiologic studies, of etiologic associations between environmental exposures and pediatric diseases; and (4) elucidation, at the cellular and molecular levels, of the pathogenetic mechanisms of pediatric environmental illness. In the United States, an important start toward adoption of this new agenda has occurred since passage of the Food Quality Protection Act in 1996. A Presidential Executive Order on Children's Health and the Environment has been promulgated. This Order requires all federal agencies to make protecting the health of children against environmental hazards a high priority. A new Office of Children's Health Protection has been established at the U.S. Environmental Protection Agency. Programs in children's environmental health have been created at the Centers for Disease Control and Prevention, the Agency for Toxic Substances and Disease Registry, and the National Institute of Environmental Health Sciences. A national network of eight new Children's Environmental Health Research and Disease Prevention Centers has been formed. These developments will enhance research on previously understudied issues in the environmental health of children and will provide a scientific basis for child-centered risk assessment.

Child↗
PubMed1999

Chemical wastes, children's health, and the Superfund Basic Research Program.

Three to 4 million children and adolescents in the United States live within 1 mile of a federally designated Superfund hazardous waste disposal site and are at risk of exposure to chemical toxicants released from these sites into air, groundwater, surface water, and surrounding communities. Because of their patterns of exposure and their biological vulnerability, children are uniquely susceptible to health injury resulting from exposures to chemical toxicants in the environment. The Superfund Basic Research Program, funded by the U.S. Environmental Protection Agency and directed by the National Institute of Environmental Health Sciences, is extremely well positioned to organize multidisciplinary research that will assess patterns of children's exposures to hazardous chemicals from hazardous waste disposal sites; quantify children's vulnerability to environmental toxicants; assess causal associations between environmental exposures and pediatric disease; and elucidate the mechanisms of environmental disease in children at the cellular and molecular level.

Child↗