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Bibliography Tag: public health

Donley et al., 2022

Donley, N., Bullard, R.D., Economos, J. et al. “Pesticides and environmental injustice in the USA: root causes, current regulatory reinforcement and a path forward”. BMC Public Health 22, 708 (2022). DOI: 10.1186/s12889-022-13057-4

ABSTRACT:

Many environmental pollutants are known to have disproportionate effects on Black, Indigenous and People of Color (BIPOC) as well as communities of low-income and wealth. The reasons for these disproportionate effects are complex and involve hundreds of years of systematic oppression kept in place through structural racism and classism in the USA. Here we analyze the available literature and existing datasets to determine the extent to which disparities in exposure and harm exist for one of the most widespread pollutants in the world – pesticides. Our objective was to identify and discuss not only the historical injustices that have led to these disparities, but also the current laws, policies and regulatory practices that perpetuate them to this day with the ultimate goal of proposing achievable solutions. Disparities in exposures and harms from pesticides are widespread, impacting BIPOC and low-income communities in both rural and urban settings and occurring throughout the entire lifecycle of the pesticide from production to end-use. These disparities are being perpetuated by current laws and regulations through 1) a pesticide safety double standard, 2) inadequate worker protections, and 3) export of dangerous pesticides to developing countries. Racial, ethnic and income disparities are also maintained through policies and regulatory practices that 4) fail to implement environmental justice Executive Orders, 5) fail to account for unintended pesticide use or provide adequate training and support, 6) fail to effectively monitor and follow-up with vulnerable communities post-approval, and 7) fail to implement essential protections for children. Here we’ve identified federal laws, regulations, policies, and practices that allow for disparities in pesticide exposure and harm to remain entrenched in everyday life for environmental justice communities. This is not simply a pesticides issue, but a broader public health and civil rights issue. The true fix is to shift the USA to a more just system based on the Precautionary Principle to prevent harmful pollution exposure to everyone, regardless of skin tone or income. However, there are actions that can be taken within our existing framework in the short term to make our unjust regulatory system work better for everyone.  FULL TEXT

Benbrook et al., 2021a

Benbrook, Charles, Perry, Melissa J., Belpoggi, Fiorella, Landrigan, Philip J., Perro, Michelle, Mandrioli, Daniele, Antoniou, Michael N., Winchester, Paul, & Mesnage, Robin; “Commentary: Novel strategies and new tools to curtail the health effects of pesticides;” Environmental Health, 2021, 20(1); DOI: 10.1186/s12940-021-00773-4.

ABSTRACT:

BACKGROUND: Flaws in the science supporting pesticide risk assessment and regulation stand in the way of progress in mitigating the human health impacts of pesticides. Critical problems include the scope of regulatory testing protocols, the near-total focus on pure active ingredients rather than formulated products, lack of publicly accessible information on co-formulants, excessive reliance on industry-supported studies coupled with reticence to incorporate published results in the risk assessment process, and failure to take advantage of new scientific opportunities and advances, e.g. biomonitoring and “omics” technologies.
RECOMMENDED ACTIONS: Problems in pesticide risk assessment are identified and linked to study design, data, and methodological shortcomings. Steps and strategies are presented that have potential to deepen scientific knowledge of pesticide toxicity, exposures, and risks.
We propose four solutions:
(1) End near-sole reliance in regulatory decision-making on industry-supported studies by supporting and relying more heavily on independent science, especially for core toxicology studies. The cost of conducting core toxicology studies at labs not affiliated with or funded directly by pesticide registrants should be covered via fees paid by manufacturers to public agencies.
(2) Regulators should place more weight on mechanistic data and low-dose studies within the range of contemporary exposures.
(3) Regulators, public health agencies, and funders should increase the share of exposure-assessment resources that produce direct measures of concentrations in bodily fluids and tissues. Human biomonitoring is vital in order to quickly identify rising exposures among vulnerable populations including applicators, pregnant women, and children.
(4) Scientific tools across disciplines can accelerate progress in risk assessments if integrated more effectively. New genetic and metabolomic markers of adverse health impacts and heritable epigenetic impacts are emerging and should be included more routinely in risk assessment to effectively prevent disease.
CONCLUSIONS: Preventing adverse public health outcomes triggered or made worse by exposure to pesticides will require changes in policy and risk assessment procedures, more science free of industry influence, and innovative strategies that blend traditional methods with new tools and mechanistic insights.

FULL TEXT

Crump et al., 2021

Crump, Casey, Groves, Alan, Sundquist, Jan, & Sundquist, Kristina; “Association of Preterm Birth With Long-term Risk of Heart Failure Into Adulthood;” JAMA Pediatrics, 2021, 175(7), 689-697; DOI: 10.1001/jamapediatrics.2021.0131.

ABSTRACT:

Preterm birth has been associated with increased risk of heart failure (HF) early in life, but its association with new-onset HF in adulthood appears to be unknown. To determine whether preterm birth is associated with increased risk of HF from childhood into mid-adulthood in a large population-based cohort. This national cohort study was conducted in Sweden with data from 1973 through 2015. All singleton live births in Sweden during 1973 through 2014 were included. Gestational age at birth, identified from nationwide birth records. Heart failure, as identified from inpatient and outpatient diagnoses through 2015. Cox regression was used to determine hazard ratios (HRs) for HF associated with gestational age at birth while adjusting for other perinatal and maternal factors. Cosibling analyses assessed for potential confounding by unmeasured shared familial (genetic and/or environmental) factors. A total of 4 193 069 individuals were included (maximum age, 43 years; median age, 22.5 years). In 85.0 million person-years of follow-up, 4158 persons (0.1%) were identified as having HF (median [interquartile range] age, 15.4 [28.0] years at diagnosis). Preterm birth (gestational age <37 weeks) was associated with increased risk of HF at ages younger than 1 year (adjusted HR [aHR], 4.49 [95% CI, 3.86-5.22]), 1 to 17 years (aHR, 3.42 [95% CI, 2.75-4.27]), and 18 to 43 years (aHR, 1.42 [95% CI, 1.19-1.71]) compared with full-term birth (gestational age, 39-41 weeks). At ages 18 through 43 years, the HRs further stratified by gestational age were 4.72 (95% CI, 2.11-10.52) for extremely preterm births (22-27 weeks), 1.93 (95% CI, 1.37-2.71) for moderately preterm births (28-33 weeks), 1.24 (95% CI, 1.00-1.54) for late preterm births (34-36 weeks), and 1.09 (95% CI, 0.97-1.24) for early term births (37-38 weeks). The corresponding HF incidence rates (per 100 000 person-years) at ages 18 through 43 years were 31.7, 13.8, 8.7, and 7.3, respectively, compared with 6.6 for full-term births. These associations persisted when excluding persons with structural congenital cardiac anomalies. The associations at ages 18 through 43 years (but not <18 years) appeared to be largely explained by shared determinants of preterm birth and HF within families. Preterm birth accounted for a similar number of HF cases among male and female individuals. In this large national cohort, preterm birth was associated with increased risk of new-onset HF into adulthood. Survivors of preterm birth may need long-term clinical follow-up into adulthood for risk reduction and monitoring for HF.

Benbrook et al., 2021

Benbrook, Charles, Kegley, Susan, & Baker, Brian; “Organic Farming Lessens Reliance on Pesticides and Promotes Public Health by Lowering Dietary Risks;” Agronomy, 2021, 11(7); DOI: 10.3390/agronomy11071266.

ABSTRACT:

Organic agriculture is a production system that relies on prevention, ecological processes, biodiversity, mechanical processes, and natural cycles to control pests and maintain productivity. Pesticide use is generally limited or absent in organic agroecosystems, in contrast with non-organic (conventional) production systems that primarily rely on pesticides for crop protection. Significant differences in pesticide use between the two production systems markedly alter the relative dietary exposure and risk levels and the environmental impacts of pesticides. Data are presented on pesticide use on organic and non-organic farms for all crops and selected horticultural crops. The relative dietary risks that are posed by organic and non-organic food, with a focus on fresh produce, are also presented and compared. The results support the notion that organic farms apply pesticides far less intensively than conventional farms, in part because, over time on well-managed organic farms, pest pressure falls when compared to the levels on nearby conventional farms growing the same crops. Biopesticides are the predominant pesticides used in organic production, which work by a non-toxic mode of action, and pose minimal risks to human health and the environment. Consequently, eating organic food, especially fruits and vegetables, can largely eliminate the risks posed by pesticide dietary exposure. We recommend ways to lower the pesticide risks by increased adoption of organic farming practices and highlight options along organic food supply chains to further reduce pesticide use, exposures, and adverse worker and environmental impacts. FULL TEXT

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