This systematic review and meta-analysis examined the impact of coke oven emissions (COEs) on respiratory health and mortality in coke production workers over a 50-year global literature (1972-2024). Polycyclic aromatic hydrocarbons (PAHs), PM2.5, benzene, and coal tar pitch volatiles (CTPVs) are the principal inhalation pollutants. The review identified 38 studies meeting inclusion criteria using a PECO framework; I-squared of 98.9% indicates substantial heterogeneity across studies.
Key numbers
- 38 studies included from initial 1,012 identified; published from 1972 to 2024.
- 47% of included studies examined effects in coke oven factory environments.
- 37% of studies focused on lung cancer, highlighting lung cancer as the top cancer concern.
- 18% of studies observed non-cancerous respiratory diseases such as COPD and chronic bronchitis, plus respiratory symptoms (chronic cough, shortness of breath).
- A statistically significant association was found between coke oven emission exposure and higher mortality from malignant respiratory diseases (95% CI for lung cancer mortality reported in meta-analysis).
- I-squared = 98.9% across studies indicates considerable variation in methodology.
- Data collection methods: questionnaires and interviews (66%), spirometry, blood/urine/sputum analysis, chest X-ray.
- Study designs from Table 2: cohort (majority), cross-sectional. Sample sizes ranged from 23 to 5,659 workers.
Methods (brief)
PECO framework: Population = coke oven plant workers; Exposure = COEs including PAHs, benzene, CTPVs, PM2.5, NO2, SO2, CO; Comparison = workers with minimal or no COE exposure; Outcomes = respiratory diseases (COPD, lung cancer, chronic bronchitis, asthma), pulmonary function (FVC, FEV1, FEV1/FVC, FEF25-75), mortality from malignant respiratory disease. Literature search: Web of Science, Scopus, PubMed, Medline, Embase through December 16, 2024. Meta-analysis of mortality: forest plot of effect sizes; Egger test for publication bias; I-squared for heterogeneity. Studies in English-language peer-reviewed journals; excluded non-English publications, conference papers, books, case reports, animal/laboratory/modeling studies, letters, editorials, short surveys.
Evidence fitness
Supports: occupational PAH and COE exposure as a cause of COPD, chronic bronchitis, asthma, and lung cancer in male industrial workers; demonstrates significant association between COE exposure and respiratory mortality. Arsenic is a component of coke oven emissions but is not the primary exposure studied. This paper documents the occupational inhalation pathway for metals, not dietary exposure. Useful for establishing that arsenic-containing industrial air pollution causes lung disease independent of diet.
Limitations
High heterogeneity (I-squared 98.9%); predominantly male populations; long historical span (1972-2024) with shifting exposure standards; mixed pollutant exposures (PAHs, PM2.5, metals, gases co-occur); arsenic-specific effects cannot be isolated from the mixture in this review.
Related evidence
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