Tag Archives: enviromental exposures

Urgent Need for New Chemical Regulations For Kids

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The Consortium for Children’s Environmental Health. NEJM 2025; 392: 299-305. Manufactured Chemicals and Children’s Health — The Need for New Law

This review article explains the worsening toll that chemicals in our environment are exacting on the health of children.

Here are some of the key excerpts:

  • “An estimated 350,000 manufactured chemicals, chemical mixtures, and plastics are currently listed in global inventories.3 Most are produced from fossil fuels — gas, oil, and coal. Production has expanded 50-fold since 1950, is currently increasing by about 3% per year, and is projected to triple by 2050.4 Environmental pollution5,6 and human exposure7 are widespread.”
  • In the past half-century, “the incidence of childhood cancers has increased by 35%.10 Male reproductive birth defects have doubled in frequency.11 Neurodevelopmental disorders now affect 1 in 6 children, and autism spectrum disorder is diagnosed in 1 in 36.12 Pediatric asthma has tripled in prevalence.13 Pediatric obesity has nearly quadrupled in prevalence and has driven a sharp increase in type 2 diabetes among children and adolescents.14 In adults, by contrast, illness, disability, and death due to cardiovascular disease, stroke, and many cancers have decreased.15,16“
  • “Research in environmental pediatrics has flourished over the past 25 years. Two key catalysts of this growth were the 1993 publication of the National Research Council report, Pesticides in the Diets of Infants and Children21 which elucidated the biologic bases of children’s heightened susceptibility to toxic chemicals, and the passage in 1996 of the Food Quality Protection Act (FQPA), the U.S. law on pesticides. The FQPA made protecting children’s environmental health a national priority and required generation of data on chemical hazards to children, stimulating substantial expansion of federally funded research in environmental pediatrics…Prenatal exposures are particularly hazardous…diseases associated with early-life exposures can manifest any time during the life span.23“
  • “Prospective, birth-cohort epidemiologic studies that measure chemical exposures in pregnant persons and fetuses and follow children longitudinally over many years are particularly powerful platforms for discovering associations between synthetic chemicals and disease because they link exposures to outcomes in individual children and eliminate recall bias.”
  • “Widespread childhood exposure to a toxic chemical can damage the health, economic viability, and security of an entire society. For example, each year from the 1950s through the 1970s, about 100,000 tons of tetraethyl lead were added to gasoline in the United States to enhance automotive performance, causing massive environmental lead contamination and extensive human exposure… The average IQ among U.S. children was reduced by an estimated 2 to 5 points,32 the number of children with an IQ above 130 decreased by more than 50%, and the number with an IQ below 70 (the criterion used in the International Classification of Diseases to define intellectual disability) increased by more than 50%…reducing toxic chemical exposures can produce major economic benefits…because each additional IQ point is associated with an increase of 1.8 to 2.4% in lifelong earning potential.
  • “Chemicals should no longer be presumed harmless until proven otherwise…National chemical policies should take into consideration findings from animal and mechanistic toxicology studies, which are highly predictive of human health risks, including risks to children.49“

My take: Pollution from chemicals and plastics is worsening and resulting in worsening health/intellectual outcomes for children. I doubt any legislation will be forthcoming to improve the situation. It is unfortunate that protecting profits is prioritized over protecting our health.

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A ‘good demon’ at The Grand Palace in Bangkok

IBD Shorts -October 2019

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Briefly noted:

D Piovani et al. Gastroenterol 2019; 157: 647-59.  This study examined environmental risk factors for inflammatory bowel disease after extensive literature review and assessment of meta-analysis.

9 factors that were associated with increased risk of IBD:

  • smoking (CD)
  • urban living (CD & IBD)
  • appendectomy (CD)
  • tonsillectomy (CD)
  • antibiotic exposure (IBD)
  • oral contraceptive use (IBD)
  • consumption of soft drinks (UC)
  • vitamin D deficiency (IBD)
  • Heliobacter species (non-Helicobacter pylori-like) (IBD)

7 factors that associated with reduced risk of IBD:

  • physical activity (CD)
  • breatfeeding (IBD)
  • bed sharing (CD)
  • tea consumption (UC)
  • high folate levels (IBD)
  • high vitamin D levels (CD)
  • H pylori infection (CD, UC, and IBD)

EL Barnes et al. Inflamm Bowel Dis 2019; 1474-80. In this review which identified 12 studies and 4843 with an IPAA ( ileal pouch-anal anastomosis) for ulcerative colitis, 10.3% were ultimately diagnosed with Crohn’s disease. Link to full text and video explanation: The Incidence and Definition of Crohn’s Disease of the Pouch: A Systematic Review and Meta-analysis

EV Loftus et al. Inflamm Bowel Dis 2019; 1522-31. In this study with 2057 adalimumab-naive patients, “the proportion of patients in HBI remission increased from 29% (573 of 1969; baseline) to 68% (900 of 1331; year 1) and 75% (625 of 831; year 6). Patients stratified by baseline immunomodulator use had similar HBI remission rates.”  Full text: Adalimumab Effectiveness Up to Six Years in Adalimumab-naïve Patients with Crohn’s Disease: Results of the PYRAMID Registry

The following study was summarized in previous blog: Oral Antibiotics For Refractory Inflammatory Bowel Disease  Full text link: Efficacy of Combination Antibiotic Therapy for Refractory Pediatric Inflammatory Bowel Disease

Washington Park, Portland, OR

What do you know about the “exposome”?

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I had not heard of the term “exposome” until last week (Gastroenterology 2012; 142: 1403-4).  However, this term was coined in 2005 (Cancer Epidemiol Biomarkers Prev 2005; 14: 1847-50).    This term is meant to describe the environmental analog of the genome.

Particularly with the gastrointestinal tract, environmental exposures are often considered a cofactor in disease development.  While there has been an increased understanding of the role of genes in the development of disease, it is abundantly clear that environment exposures can independently cause disease or act as a ‘second hit.’  The gastrointestinal tract is exposed to fluids which contain a multitude of elements and microorganisms, and to foods with their variability in nutrients, microbes and pollutants.  Other environmental factors include smoking, ionizing radiation, noise, breastfeeding, medications, and antimicrobials.

This cited commentary explains how environmental scientists are trying to unravel the ‘exposome.’

  • Bottom-up strategy:  measure external sources of the individual exposome at multiple time points.  This strategy may benefit from improvement in informatics, remote & personal sensing devices.
  • Top-down strategy: examines internal milieu including blood, biologic specimens, and transcriptomics/proteonomics.  Early examples include distinct signatures associated with specific environmental exposures.

Both strategies require validation to understand how external exposures trigger internal changes and disease expression.  Promising fields in gastroenterology for the study of the exposome include IBD, gastrointestinal cancers, functional disorders, and even obesity.  It is likely that studies of the exposome will answer questions about why the frequency of so many diseases are changing much more readily than studies of the genome.

Related blog posts:

Eat your veggies…if you don’t want to get sick

Why are we seeing so many more cases

Additional references:

  • -PLoS One 2010; 5 e10746.  Novel associations between type 2 diabetes and specific chemical exposures.
  • -Nature 2006; 444: 1027-31.  Obesity-associated gut microbiome.
  • -BMC Med Genomics 2010; 3: 17.  Chemical factors associated with disease-related gene expression data.