ENVIRONMENTAL CARCINOGENESIS IN HARYANA, INDIA: A CRITICAL COMPREHENSIVE REVIEW OF CANCER SURVEILLANCE, MULTIEXPOSURE PATHWAYS, AND PREVENTION PRIORITIES
Jul 2026· International Journal of Engineering Applied Sciences and Technology· Vol 11, pp. 96-112· 0 citations
TL;DR
A transparent evidence hierarchy, an eco-oncology framework, districtcluster research priorities, and an implementation roadmap centred on sustained population-based cancer registration, historical exposure reconstruction, safe water, clean air, pesticide stewardship, and worker protection are proposed.
Abstract
Haryana combines rapid industrialisation,
intensive agriculture, severe air pollution, groundwater
stress, and uneven occupational and environmental
regulation, creating a plausible setting for cumulative
carcinogenic exposure. This critical comprehensive review
integrates cancer surveillance, Haryana-specific
environmental studies, institutional monitoring,
mechanistic evidence, and international epidemiology while
distinguishing hazard detection from demonstrated local
causation. ICMR-NCRP estimates indicate that annual
incident cancer cases increased from 29,219 in 2020 to
32,513 in 2024. The peer-reviewed Haryana Cancer Atlas
analysis included 36,736 confirmed cancers diagnosed in
2016-2017 from 126 participating centres, supplemented by
eligible records from 28 hospital-based cancer registries,
and identified substantial district and site-specific
variation. The broader administrative atlas reported
42,699 records from 149 sources, illustrating why analytic
and administrative totals should not be conflated. Rohtak
had the highest male all-site age-adjusted incidence rate
(143.9 per 100,000), whereas Gurugram had the highest
female rate (108.2); high head-and-neck cancer rates
among men and district variation in breast, lung, prostate,
and cervical cancer require targeted surveillance but do
not establish environmental causation. Groundwater
monitoring identified nitrate, fluoride, arsenic, and
uranium exceedances, while pesticide residues, industrial
mixtures, ambient particulate matter, combustion
emissions, and workplace exposures create additional
prevention priorities. The strongest causal evidence
relevant to Haryana concerns outdoor air pollution,
benzene, inorganic arsenic, hexavalent chromium,
cadmium, and selected occupational exposures; pesticide
evidence remains compound- and outcome-specific, and
uranium requires cautious interpretation because its
drinking-water guideline primarily reflects chemical
nephrotoxicity. The review proposes a transparent
evidence hierarchy, an eco-oncology framework, districtcluster research priorities, and an implementation
roadmap centred on sustained population-based cancer
registration, historical exposure reconstruction, safe water,
clean air, pesticide stewardship, and worker protection.
Haryana offers a transferable model for environmentalcancer surveillance in rapidly industrialising,
agriculturally intensive, data-constrained regions.
Background: Occupational cancer represents a major but underrecognized public health challenge, contributing to an estimated 8% of global cancer cases. Workers in high-risk industries, such as construction, chemical manufacturing, and mining, face prolonged exposure to carcinogens including asbestos, benzene, and aromatic amines.
Objectives: This review examines the role of occupational medicine in identifying, managing, and preventing cancers linked to workplace exposures, while addressing diagnostic advances, regulatory frameworks, and preventive strategies.
Methods: A narrative review of existing literature, regulatory documents, and surveillance data was conducted, focusing on biological mechanisms of carcinogenesis, industry-specific risks, diagnostic innovations, and prevention policies.
Results: Occupational carcinogenesis involves mechanisms such as genotoxicity, oxidative stress, epigenetic alterations, and chronic inflammation. Key carcinogens include vinyl chloride and chromium VI. Advances in biomarker analysis and health surveillance enhance early detection and risk assessment. Regulatory measures, ranging from IARC classifications to national compensation laws, provide frameworks for protection but face implementation barriers, especially in low- and middle-income countries. Preventive strategies based on the hierarchy of controls, health education, and green chemistry remain central, while emerging concerns include underreporting, nanoparticle exposure, and psychosocial impacts.
Conclusions: A multidisciplinary approach is essential for reducing the burden of occupational cancer. Future directions include digital surveillance systems, personalized occupational medicine, and stronger global collaborations to ensure workplace safety and equitable health outcomes.
Dhanya Boopathe, Kamalesh V· Adolescência e Saúde· 0 citations
An increase in formaldehyde concentration in the air is associated with a gain in breast cancer incidence, especially at the early stages, and it is advisable to strengthen formaldehyde monitoring, implement molecular epidemiological screening of these polymorphisms and active detection of breast cancer in genetically determined risk groups.
O. N. Gulyaeva, Ivan E. Tereshkin, V. Kislitsyna et al.· Hygiene and Sanitation· 0 citations
High-molecular-weight carcinogens significantly accumulate in human lungs in Northern Thailand, reflecting substantial environmental exposure, while tissue lipid content modulates toxin bioaccumulation, underscores an urgent need for targeted public health strategies addressing both environmental pollution and tobacco use.
The deterioration of ambient air quality worldwide has intensified the need to examine the environmental factors associated with the growing burden of respiratory disease. This study aimed to identify broad patterns in the adverse effects of environmental exposures on the respiratory system, while accounting for regional variation and population-specific vulnerability. A systematic literature review was conducted between April and December 2024 using four international databases: PubMed, Web of Science, Scopus, and Google Scholar. Seventy-one relevant publications were included in the final analysis. The findings indicate that, in India, concentrations of particulate matter with aerodynamic diameters of up to 10 μm (PM₁₀) and 2.5 μm (PM₂.₅) exceed recommended limits by a factor of 2.56. In Northern Thailand, reductions of 5.3%–34.3% in particulate matter concentrations were associated with significant declines in hospitalization rates. In China and South Africa, pollutant levels substantially exceed the World Health Organization guideline of 5 μg/m³, while national standards in some settings permit concentrations of up to 40 μg/m³, thereby increasing the risk of chronic inflammatory respiratory conditions. In Bogotá, Colombia, heavy traffic contributes to increased morbidity and mortality from respiratory complications. In Kyrgyzstan, seasonal variation and changes in vegetation patterns have been linked to a rise in allergic reactions, whereas in Slovakia, prolonged pollen seasons are associated with a higher prevalence of bronchial asthma. Children, particularly those under 5 years of age, older adults, and industrial workers were identified as the most vulnerable groups. Climate change further aggravates these risks by intensifying exposure to fine particulate matter and gaseous pollutants. The findings underscore the need for integrated policies focused on emission reduction, environmental monitoring, public awareness, and the harmonization of air-quality standards. The study provides evidence that may support cross-sectoral planning and the development of preventive strategies aimed at reducing the burden of acute and chronic respiratory disease.
Zhanibek Muratov, Aida Zotaj, A. Kalandarova et al.· Luna Azul· 0 citations
Arsenic is a widespread environmental metalloid whose inorganic forms contaminate drinking water, food chains, soil and air. Male reproductive toxicity is biologically plausible because spermatogenesis, steroidogenesis and post-testicular sperm maturation depend on tightly regulated redox, metabolic and endocrine processes. Yet the evidential basis for attributing human male subfertility to environmental arsenic remains markedly less secure than the experimental literature might suggest. This critical narrative review integrates exposure science, human epidemiology, animal and cell-model evidence, mechanistic research and methodological limitations. Literature published from 1980 to 1 June 2026 was identified through PubMed/MEDLINE, authoritative institutional websites and supplementary scholarly web searching, with backward and forward citation checking. Human studies provide signals of lower sperm concentration or motility, altered seminal biomarkers, infertility-associated urinary arsenic species and perturbation of steroid-hormone excretion. These findings are not uniform: studies are few, often clinic-based and cross-sectional, and differ in arsenic speciation, exposure range, co-exposures, semen assessment and confounder control. Experimental evidence is more coherent, linking arsenite and related compounds to oxidative injury, mitochondrial dysfunction, germ-cell loss, impaired spermatid elongation, acrosomal and flagellar defects, epididymal dysfunction, endocrine disruption, autophagy and altered sperm proteins. Developmental exposure and incomplete recovery after withdrawal raise concern about vulnerable windows, although doses and species frequently limit direct translation to human environmental exposure. The strongest current inference is that arsenic can damage male reproductive biology and may contribute to impaired semen quality in susceptible or highly exposed populations; the magnitude of risk at common low-level exposure is uncertain. Progress requires prospective preconception cohorts, repeated arsenic speciation and semen sampling, mixture-aware analysis, functional sperm and fertility outcomes, and explicit evaluation of reversibility after exposure reduction. Prevention should prioritise exposure control rather than unvalidated arsenic-specific fertility treatments.
S. K. Nayak, B. Behra, Mohammed Shoeb et al.· Asian Journal of Biology· 0 citations
BACKGROUND AND OBJECTIVE
Formaldehyde (FA), classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC), constitutes a significant occupational hazard within hospital pathology service, where it remains the "gold standard" fixative for tissue preservation. Despite widespread recognition of its toxicological properties, the specific carcinogenic and non-carcinogenic health risks confronting pathology personnel subjected to chronic, low-level, and intermittent exposures remain incompletely characterized. This review synthesizes the current body of evidence regarding the cellular and molecular mechanisms of FA toxicity, histopathological (HP) alterations in target tissues, and associated occupational health risks among pathology staff. Study selection for review: A comprehensive literature search was conducted across PubMed∕MEDLINE, Web of Science, and Scopus databases, encompassing publications through December 2025. Studies were selected based on relevance to FA toxicity mechanisms, HP effects, and occupational exposure in pathology settings. Given the heterogeneity of study designs and outcomes, a narrative synthesis approach was adopted.
EVIDENCE SYNTHESIS
The synthesized evidence demonstrates that pathology personnel are routinely exposed to FA concentrations exceeding recommended occupational exposure limits (OELs). At the cellular level, FA exerts toxicity through deoxyribonucleic acid (DNA)-protein crosslink formation, oxidative stress induction, and inflammatory pathway activation. HP examination of exposed individuals reveals a characteristic progression from ciliary loss and goblet cell hyperplasia through squamous metaplasia to epithelial dysplasia in the nasal mucosa. Non-carcinogenic health effects, including respiratory symptoms and genotoxicity biomarker elevation, are highly prevalent. However, direct epidemiological evidence substantiating elevated cancer risk within this specific occupational cohort remains limited, mainly due to improper (occupational medicine) reporting.
CONCLUSIONS
This review confirms substantial non-carcinogenic health effects among pathology personnel, with documented HP alterations representing preneoplastic changes at the portal of entry. The mechanistic evidence supports biological plausibility for carcinogenic risk, though epidemiological confirmation specific to this workforce remains lacking, highlighting a critical research gap.
M. Șerbănescu, A. Rotaru-Zăvăleanu, Lucrețiu Radu· Romanian journal of morpholo...· 0 citations