Occupational Exposures in the Painting Industry

Painting Process Exposure

Chemicals: Workers are exposed to various chemicals found in paint products during application and removal processes.

Specific Exposures: Dichloromethane during paint stripping, diisocyanate in binders, silica in surface preparation, asbestos, and crystalline silica as bystanders during construction or demolition.

Exposure Routes: Inhalation and skin contact during manual handling, preparation, mixing, thinning, tinting, shading, and cleaning processes.

Types of Exposures

Solvents: During paint application.

Pigments and Fillers: During mechanical paint removal.

Other Exposures: Emissions of various substances during varnish cooking and production processes.

Protective Measures

Personal Protective Equipment (PPE): While PPE can reduce exposure, painters often do not wear respirators or gloves.

Nanoparticles: Use of nanoparticles in paint (0.5–5% w/w) improves properties, but exposure to individual nanoparticles is minimal due to agglomeration and incorporation into the polymer matrix.

Health Risks Associated with Painting Occupations

Cancer Risks

Lung Cancer: Painters have an increased risk of lung cancer. Cohort and case–control studies consistently show elevated risks, even after adjusting for smoking.

Mesothelioma: Painters also have an increased risk of mesothelioma, further suggesting asbestos exposure.

Urinary Bladder Cancer: There is a consistent increase in the incidence of bladder cancer among painters, supported by both cohort and case–control studies.

Childhood Leukaemia: Maternal Exposure: Positive associations were found between maternal exposure during painting and childhood leukaemia, indicating a potential risk factor. Paternal Exposure: Limited evidence suggests a positive association between paternal exposure and childhood leukaemia.

Lympho-haematopoietic Cancers: Inconsistent results were observed, making it difficult to draw conclusions regarding the association between painting occupations and lymphatic and haematopoietic cancers

Toxicokinetics and Metabolism of Paint Components


(a) Aromatic Hydrocarbons:

  • Benzene: For detailed toxicokinetics of benzene, please refer to the Monograph on Benzene in this volume.
  • Toluene: Metabolized to benzyl alcohol and subsequently oxidized to benzoic acids, excreted as conjugates with glycine or UDP-glucuronate.
  •  Xylene: Metabolized to methylbenzyl alcohol, forming methylhippuric acid conjugates with glycine. Limited aromatic hydroxylation to xylenol observed in humans.


(b) Chlorinated Solvents:

  • Dichloromethane (DCM): Mainly absorbed via inhalation, metabolized by CYP2E1 enzyme. Pathways yield formyl chloride, CO, CO2, and formaldehyde. Elimination occurs mainly through expired air and urine.
  •  Trichloroethylene (TCE): Absorbed primarily through inhalation, widely distributed in liver, kidneys, cardiovascular, and nervous systems. Metabolized through oxidative pathways by various CYP isoenzymes and conjugation with glutathione, leading to the formation of toxic metabolites.

Metals in Paints:


  • Absorption: Mainly through inhalation in the workplace; general population exposure through food and water.
  • Distribution: Binds to metallothionein and is transported to liver and kidneys via blood.
  • Excretion: Primarily via urine, with a half-life in the body estimated to be 7-16 years.



  • Absorption: Depends on solubility and particle size; higher for chromium (VI) compounds; occurs in lungs and gastrointestinal tract.
  • Distribution: Found in all organs, with highest concentrations in kidneys, liver, and bone.
  • Excretion: Via urine after inhalation and via feces after oral exposure.


Lead Compounds:

  • Absorption: Through inhalation, oral, or dermal exposure; settled deep in lungs is eventually absorbed; dermal absorption is negligible.
  • Distribution: Rapidly distributed in the body, especially in bone.
  • Excretion: Primarily in urine and via bile in feces.


Other Compounds in Paints:


  • Absorption: Rapid distribution in the body, highest concentrations in adipose tissue.
  • Metabolism: Converted to styrene-7,8-oxide, excreted as urinary mandelic and phenylglyoxylic acids.
  • PAHs (Polycyclic Aromatic Hydrocarbons):
  • Exposure: Occurs through waterproof coatings or pyrolysis of paint residues.
  • Toxicokinetics: Limited data; generally occur as complex mixtures; specifics vary among different



Aromatic Amines and Azo Dyes

Toxicokinetics: Described in specific IARC Monograph volumes.

Genetics and Related Effects in Painters

Genetic Effects of Individual Paint Constituents

(a) Benzene: Refer to the dedicated Monograph section on Benzene for detailed information on its genetic effects.

(b) Toluene: Toluene exposure in workers exhibited inconclusive human genotoxicity results due to various limitations in study design and methodology. Nonetheless, some studies reported increases in chromosomal aberrations, micronuclei, and DNA strand-breaks (Chen et al., 2008). In experimental setups, toluene co-exposure with benzene enhanced clastogenic or aneugenic bone-marrow injury in mice, indicating potential synergistic effects (Wetmore et al., 2008).

(c) Xylene: Studies on xylenes displayed negative genotoxic results in various in vitro and in vivo assays. Indirect DNA fragmentation occurred at cytotoxic concentrations, suggesting genotoxicity might be mediated by cell death mechanisms (ATSDR, 2007b).

(d) Dichloromethane: Dichloromethane demonstrated consistent mutagenicity in microorganisms and exhibited various responses in mammalian systems. Dichloromethane-induced genotoxic effects in human cells suggested potential carcinogenic mechanisms, primarily linked to GST-mediated metabolism (IARC, 1999).

(e) Trichloroethylene: Exposure to trichloroethylene (TCE) demonstrated clastogenic effects, with increased micronuclei and DNA single-strand breaks observed in rodents. Although TCE itself might not be genotoxic, its reactive metabolites raised concerns, indicating potential genetic toxicity (ATSDR, 1997).

 (f) Cadmium and Chromium: Refer to Monograph Volume 100C for detailed genetic effects of cadmium and chromium.

 (g) Inorganic Lead: Lead exposure correlated with DNA strand-breaks, chromosomal aberrations, and micronuclei. The genotoxicity of lead was attributed to disruption of pro-oxidant/antioxidant balance and interference with DNA-repair systems, mediated through oxidative stress pathways (IARC, 2006).

(h) Styrene: Styrene exposure led to DNA adduct formation, particularly in humans. While mice developed lung tumors, the mechanism, potentially involving styrene 7,8-oxide, may not be significant in human lungs. Nevertheless, DNA adducts and chromosomal damage were observed in human workers, suggesting multiple mechanisms might be at play (IARC, 2002).

(i) PAHs: PAHs demonstrated genotoxic effects, primarily attributed to benzo[a]pyrene. Metabolic activation of PAHs led to the formation of DNA adducts, posing significant risks in human exposure scenarios (IARC, 2010d).

(j) Aromatic Amines and Azo Dyes: Refer to Monograph Volume 99 for detailed information on the genotoxic effects of aromatic amines and azo dyes.

Indirect Effects Potentially Related to Genotoxicity

Beyond direct genotoxicity, painters exhibited hematological changes, including altered white blood cell levels, and immunological responses to specific substances, further highlighting the complex and multi-faceted impacts of paint exposure on human health.