Occurrence and dietary exposure assessment of pentachlorophenol in livestock, poultry, and aquatic foods marketed in Guangdong Province, China: Based on food monitoring data from 2015 to 2018.

As a persistent organic pollutant, pentachlorophenol (PCP) has serious impacts on human health. However, its presence in animal source food products sold in the Guangdong Province (GD) of China, and the resultant dietary exposure have not been elucidated. To address this gap, 3,100 samples from seven food categories, including beef, pork, mutton, offals, broilers, hen eggs, and farmed freshwater fish, marketed throughout four geographical regions of GD, were collected from 2015 to 2018. Gas chromatography coupled with mass spectrometry was employed to detect PCP levels in these food matrices. PCP was found in all food categories, but the average contamination levels were low, ranging from 0.40 µg/kg wet weight (ww) (hen eggs) to 5.85 µg/kg ww (offals). However, higher concentrations of PCP were detected (P < 0.05) in animal source food from the North region. Additionally, a temporal declining trend was observed in this four-year consecutive survey. The estimated human dietary exposure of PCP to population groups, including the general population and subgroups (male and female, children, and adults), was found to be far below the permissible daily intake (3 µg/kg body weight). Therefore, the health impacts of PCP should be correspondingly low for local residents, based on current toxicological knowledge. Regional exposure patterns varied due to different extents of contamination in the four areas, and pork, broilers, and freshwater fish were the major sources of dietary PCP exposure. PRACTICAL APPLICATION: As a persistent organic pollutant, pentachlorophenol (PCP) has serious impacts on human health. However, its presence in animal source food products sold in Guangdong Province of China, and the resultant dietary exposure have not been elucidated. In this study, we conducted an in-depth investigation on the occurrence of PCP in major foodstuff categories, including beef, pork, mutton, broilers, offals, hen eggs, and farmed freshwater fish, marketed in all 21 prefecture-level divisions of Guangdong Province, in order to provide integral insights for regulatory authorities.

The European water-based environmental quality standard for pentachlorophenol is NOT protective of benthic organisms.

Risk management of toxic substances is often based on Environmental Quality Standards (EQS) set for the water compartment, assuming they will also protect benthic organisms. In the absence of experimental data, EQS for sediments can be estimated by the equilibrium partitioning approach. The present study investigates whether this approach is protective of benthic organisms against pentachlorophenol (PCP), a legacy contaminant and EU priority substance still used in some parts of the world. Three freshwater species of invertebrates with different life cycles and feeding behaviors (the oligochaetes Lumbriculus variegatus, Tubifex tubifex and the dipteran insect Chironomus riparius) were exposed to PCP spiked sediments (2.10-46.03mgPCP/kg d.w. plus controls) in laboratory standard tests. Exposure duration was 28days for T. tubifex and L. variegatus and 10 and 28days for C. riparius; according to the corresponding OECD guidelines. For each investigated end-point, dose-response data were normalized to the mean control and fitted to a four-parameter log-logistic model for calculating the corresponding EC50 and EC10. The ranges for EC50 and EC10 estimates were 4.39 (Chironomus riparius-emergence)-27.50 (Tubifex tubifex-cocoon) and 0.30 (T. tubifex-young worms) -16.70 (T. tubifex-cocoon) mg/kg d.w., respectively. The EC50 and the EC10 values of L. variegatus were within these ranges. Following the EU Technical Guidance for deriving EQS, the lowest EC10 value of 0.30mg/kg (T. tubifex-young worms) resulted in a PCP quality standard (QS) for sediments of 30ng/g, about one fourth of the tentative QS of 119ng/g estimated by the equilibrium partitioning (EqP) approach. The response of benthic biota to PCP varied across organisms and across end-points for the same organism, so that the use of sediment PCP-QS calculated using the EqP-approach may be under-protective of the most sensitive organisms. Information on the possible effects of PCP on resident organisms must therefore be collected for appropriately managing aquatic systems.

Evaluation of Complex Toxicity of Canbon Nanotubes and Sodium Pentachlorophenol Based on Earthworm Coelomocytes Test.

As a standard testing organism in soil ecosystems, the earthworm Eisenia fetida has been used widely in toxicity studies. However, tests at the individual level are time- and animal-consuming, with limited sensitivity. Earthworm coelomocytes are important for the assimilation and elimination of exogenous compounds and play a key role in the processes of phagocytosis and inflammation. In this study, we explored an optimal condition to culture coelomocytes of E. fetida in vitro and investigated the cytotoxicity of multiwalled carbon nanotubes (MWCNTs) and sodium pentachlorophenol (PCP-Na) using coelomocytes via evaluating lethal toxicity, oxidative stress, membrane damage, and DNA damage. The results showed that coelomocytes can be successfully cultured in vitro in primary under the RPMI-1640 medium with 2-4×104 cells/well (1-2×105 cells/mL) in 96-well plates at 25°C without CO2. Both MWCNTs and PCP-Na could cause oxidative damage and produce ROS, an evidence for lipid peroxidation with MDA generation and SOD and CAT activity inhibition at high stress. The two chemicals could separately damage the cell membrane structure, increasing permeability and inhibiting mitochondrial membrane potential (MMP). In addition, our results indicate that PCP-Na may be adsorbed onto MWCNTs and its toxicity on earthworm was accordingly alleviated, while a synergetic effect was revealed when PCP-Na and MWCNTs were added separately. In summary, coelomocyte toxicity in in vitro analysis is a sensitive method for detecting the adverse effects of carbon nanotubes combined with various pollutants.

Historical long-term exposure to pentachlorophenol causing risk of cancer--a community study.

BACKGROUND: Pervious studies suggested occupational workers exposure to pentachlorophenol (PCP) might contribute to increased risk of cancer. However, few studies have focused on associations between PCP and cancer risk at the community level. OBJECTIVE: The present study was to explore the cancer risk for the community population living long-term in a PCP contaminated area. METHODS: All the cancer cases diagnosed in 2009- 2011 in Tongling City were collected. The cancer patients' residencies were geo-referenced in each district. The historical PCP usage for each district of Tongling was calculated as the PCP pollution index, which was further used to divide into PCP exposure categories. Standardized rate ratios (SRRs) of cancer incidence were applied to detect the cancer risk as exposure grade elevated. Correlation analysis was performed to analyze the relationship between PCP pollution and cancer incidence. RESULTS: A total of 5,288 cancer cases (3,451 male and 1,837 female) were identified. PCP usage was correlated with the incidence of leukemia (r=0.88, P=0.002) for males, and with cancer of the esophagus for males (r=0.83, P=0.008) and females (r=0.71, P=0.020). Compared with the low exposure category, significant SRRs for total cancer sites was obtained for high PCP exposure category (SRR=1.61, 95%CI=1.59-1.62). Most SRR values of the cancer sites were significantly increased as exposure grade elevated and exposure time extended. CONCLUSION: The present study found that community residents living in the PCP contaminated area had increased risk of cancers. Leukemias, lymphomas and nasopharyngeal and esophageal cancers are most possibly associated with PCP exposure.

Biochemical study of retired pentachlorophenol workers with and without following dietary exposure to PCDD/Fs.

PCDD/Fs are found as impurities in commercial pesticide sodium pentachlorophenol (Na-PCP) salt. We compared, using multivariate logistic regression analysis adjusted for confounding factors, serum PCDD/F levels and biochemical examinations of retired Na-PCP workers and other inhabitants living near a closed Na-PCP plant that discharged PCP-contaminated wastewater into a nearby pond in Tainan, Taiwan. In this cross-sectional study from October 2006 through May 2009, 1167 participants were divided into groups according to their occupational (retired Na-PCP plant workers versus other residents) and dietary exposure (eating polluted fish versus not eating polluted fish) to PCDD/Fs, and a general population from a large-scale survey. Serum PCDD/F levels were significantly different between these groups (range: from 22.9±10.0pg WHO(98)-TEQ(DF) g(-1) lipid in the general population to 109.6±94.5pg WHO(98)-TEQ(DF) g(-1) lipid in retired Na-PCP workers eating polluted seafood; P(trend)<0.001). Distinct patterns of PCDD/Fs congener profiles, showing a significantly higher proportion of 1,2,3,7,8-PeCDD, 1,2,3,6,7,8-HxDD, and less 2,3,4,6,7,8-HpCDF, OCDF, were also found among workers and residents with different serum PCDD/F levels versus the general population. After adjusting for confounding factors, glucose (adjusted odds ratio [AOR] 7.22 [95% CI: 4.04-12.90]), triglycerides (AOR 4.31 [95% CI: 2.57-7.22]), blood urea nitrogen (AOR 2.90 [95% CI: 1.58-5.33]), creatine (AOR 5.83 [95% CI: 1.12-30.30]) and total protein (AOR 3.74 [95% CI: 1.91-7.31]) levels in retired workers were significantly higher than in the reference group. Occupational exposure to PCDD/Fs is associated with biochemical abnormalities that may persist for years after serum PCDD/F levels have declined.

Mortality rates among trichlorophenol workers with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The authors examined 1,615 workers exposed to dioxins in trichlorophenol production in Midland, Michigan, to determine if there were increased mortality rates from exposure. Historical dioxin levels were estimated by a serum survey of workers. Vital status was followed from 1942 to 2003, and cause-specific death rates and trends with exposure were evaluated. All cancers combined (standardized mortality ratio (SMR) = 1.0, 95% confidence interval (CI): 0.8, 1.1), lung cancers (SMR = 0.7, 95% CI: 0.5, 0.9), and nonmalignant respiratory disease (SMR = 0.8, 95% CI: 0.6, 1.0) were at or below expected levels. Observed deaths for leukemia (SMR = 1.9, 95% CI: 1.0, 3.2), non-Hodgkin lymphoma (SMR = 1.3, 95% CI: 0.6, 2.5), diabetes (SMR = 1.1, 95% CI: 0.6, 1.8), and ischemic heart disease (SMR = 1.1, 95% CI: 0.9, 1.2) were slightly greater than expected. No trend was observed with exposure for these causes of death. However, for 4 deaths of soft tissue sarcoma (SMR = 4.1, 95% CI: 1.1, 10.5), the mortality rates increased with exposure. The small number of deaths and the uncertainty in both diagnosis and nosology coding make interpretation of this finding tenuous. With the exception of soft tissue sarcoma, the authors found little evidence of increased disease risk from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The environmental behaviour of polychlorinated phenols and its relevance to cork forest ecosystems: a review.

Pentachlorophenol (PCP) has been used as a herbicide, biocide and preservative worldwide since the 1930s and as a result, extensive and prolonged contamination exists. The environmental impact increases when its many degradation products are taken into consideration. A number of chloroanisols and their related chlorophenols have been found in cork slabs collected from Portuguese oak tree forests before stopper manufacturing, and contamination by PCP and polychlorinated anisole (PCA) has been detected in Canadian forests. It is suggested that the use of polychlorinated phenols, in particular PCP, is thought to be a cause of the cork taint problem in wine, a major socio-economic impact not only for industry but on sensitive and highly biodiverse ecosystems. It also highlights particular issues relating to the regional regulation of potentially toxic chemicals and global economics world wide. To fully understand the impact of contamination sources, the mechanisms responsible for the fate and transport of PCP and its degradation products and assessment of their environmental behaviour is required. This review looks at the current state of knowledge of soil sorption, fate and bioavailability and identifies the challenges of degradation product identification and the contradictory evidence from field and laboratory observations. The need for a systematic evaluation of PCP contamination in relation to cork forest ecosystems and transfer of PCP between trophic levels is emphasised by discrepancies in bioaccumulation and toxicity. This is essential to enable long term management of not only transboundary contaminants, but also the sustainable management of socially and economically important forest ecosystems.

Impact of the specificity of the exposure metric on exposure-response relationships.

BACKGROUND: Exposure misclassification may occur when nonspecific exposure indicators are used. Developing estimates of more specific measures may be difficult due to sampling limitations or a paucity of historical measurements and, thus, often requires substantial effort. We examine the impact on exposure-response relationships of moving from 2 measures of exposure mixtures (dust, chlorophenols) to more specific exposure indicators (wood dust, pentachlorophenol, tetrachlorophenol) in a retrospective cohort. METHODS: The study population consisted of 26,847 male sawmill workers (> or =1 year employment between 1950 and 1995) with linkage to national cancer registries. A subcohort (n = 11,273 employed more than 1 day between 1985 and 1995) was linked to hospital discharge records. We evaluated the shape (log-linear vs log-log models), goodness of fit, precision, and expected versus observed attenuation of the exposure-response relationships. RESULTS: The correlation between the cumulative exposure indices was moderately high (dust/wood dust, r = 0.68; total chlorophenol/pentachlorophenol, r = 0.88; total chlorophenol/tetrachlorophenol, r = 0.78). An increase in chronic obstructive pulmonary disease hospitalizations was found with wood dust but not with total dust. Stronger associations for non-Hodgkin lymphoma and kidney cancer incidence were observed with pentachlorophenol than with total chlorophenol; no association was observed with tetrachlorophenol. We observed greater attenuation than expected using total dust, but less than expected using total chlorophenol. CONCLUSIONS: The relationships between health outcomes were substantially attenuated when nonspecific exposure indicators were used. This study demonstrates the importance of developing exposure metrics as specific to the disease-causing agent as possible, particularly when the composition of mixed exposures varies by work areas.

Health effects on nearby residents of a wood treatment plant.

OBJECTIVES: The aim of the study was to evaluate the health status of nearby residents of a wood treatment plant who had sustained prolonged low-level environmental exposure to wood processing waste chemicals. METHODS: A population of 1269 exposed residents who were plaintiffs or potential plaintiffs in a lawsuit against the wood treatment plant were evaluated by questionnaire for a health history and symptoms. A representative sample of 214 exposed subjects was included in the analysis. One hundred thirty-nine controls were selected from 479 unexposed volunteers and matched to the exposed subjects as closely as possible by gender and age. Subjects and controls completed additional questionnaires and were evaluated by a physician for medical history and physical examination, blood and urine testing, neurophysiological and neuropsychological studies, and respiratory testing. Environmental sampling for wood processing waste chemicals was carried out on soil and drainage ditch sediment in the exposed neighborhood. RESULTS: The exposed subjects had significantly more cancer, respiratory, skin, and neurological health problems than the controls. The subjective responses on questionnaires and by physician histories revealed that the residents had a significantly greater prevalence of mucous membrane irritation, and skin and neurological symptoms, as well as cancer. (Exposed versus unexposed, cancer 10.0% versus 2.08%, bronchitis 17.8% versus 5.8%, and asthma by history 40.5% versus 11.0%) There were significantly more neurophysiologic abnormalities in adults of reaction time, trails A and B, and visual field defects. CONCLUSIONS: Adverse health effects were significantly more prevalent in long-term residents near a wood treatment plant than in controls. The results of this study suggest that plant emissions from wood treatment facilities should be reduced.

Environmental agents as cause of health disorders in children presented at an outpatient unit of environmental medicine.

There are no publications on the frequency of environmental agents causing diseases in children presented at centers of environmental medicine. The aim of this study was to perform a statistical analysis of the data of children who visited the outpatient Unit of Environmental Medicine (UEM) at the University Hospital of Aachen, Germany. Data of all UEM patient files from January 1988 to September 1996 were evaluated. From a total of 682 patients, 75 were children (40 girls, 35 boys, age range 1-12 years). Forty-six children were presented with unspecific health disorders, 12 to examine a possible relationship between environmental agents and a current condition, mostly atopy (n = 10). Complaints were mucosal irritations (n = 38), unspecific (n = 19), dermatological (n = 16), gastrointestinal (n = 4), heart/circulation-related (n = 2), musculoskeletal (n = 1) and neurological (n = 1) symptoms. Wood preservatives were mentioned as suspected environmental causative agents in 22 cases, followed by unspecific indoor factors (n = 15), factories/disposal sites near homes (n = 9), formaldehyde (n = 5) and unspecific exposures (n = 5). Biomonitoring was done in 44 cases, local inspections and ambient monitoring in 10 cases. No evidence for a cause-and-effect relationship was found in 55 children, but was deemed possible in nine cases. In nine other children, a relatively high degree of exposure was determined by chemical analysis, but clinical relevance remained unclear. One child suffered from subclinical mercury poisoning caused by inadequate homeopathic medication. In most children referred to an environmental medicine center, it is difficult or impossible to verify an environmental cause using the diagnostic instruments currently available.

Effects of pentachlorophenol and tetrachlorohydroquinone on mitogen-activated protein kinase pathways in Jurkat T cells.

When Jurkat human T cells were incubated with 20 microM of pentachlorophenol (PCP) or its metabolite, tetrachlorohydroquinone (TCHQ), for 10 hr, flow cytometric analyses revealed marked increase in the number of apoptotic cells. DNA fragmentation was also observed in these cells. TCHQ was more potent than PCP in causing apoptosis. After incubation with 20 microM TCHQ for 1 hr, all mitogen-activated protein kinases (MAPKs) examined [i.e., extracellular signal-regulated protein kinase (ERK), p38, and c-Jun NH(2)-terminal kinase (JNK)] were phosphorylated, whereas no clear phosphorylation was induced by PCP. TCHQ-induced apoptosis was markedly suppressed by treatment with a p38 inhibitor (SB203580) and mildly (but significantly) suppressed by treatment with a MAPK/ERK kinase inhibitor (U0126). When cells were treated with both inhibitors at the same time, TCHQ-induced apoptosis disappeared almost completely. PCP-induced apoptosis was also suppressed by SB203580 and/or U0126. Nevertheless, treatment with LL-Z1640-2, which inhibits JNK phosphorylation, did not suppress the apoptosis caused by either TCHQ or PCP. Thus, p38 and ERK appear to be important signal transduction pathways leading to apoptosis in a human T-cell line exposed to a ubiquitous pollutant or its metabolite in the general and occupational environment.

Proliferation and differentiation of murine haemopoietic progenitor cells in stroma-free culture in the presence of metabolites of chlorinated pesticides.

We have studied the influence of metabolites of chlorinated pesticides (lindane, pentachlorophenol, hexachlorobenzene) on proliferation and differentiation in two stroma-free murine bone marrow culture models, a multipotent progenitor cell line (FDCP-mix) and primary lineage-depleted bone marrow cells. Tetrachlorohydroquinone (Cl(4)pHQ), tetrachloro-p-benzoquinone (Cl(4p)BQ), but not their positional isomers, tetrachlorocatechol (Cl(4)oHQ) and tetrachloro-o-benzoquinone (Cl(4)oBQ), nor 2,4,6-trichlorophenol (2,4,6-Cl(3)P), were much more toxic to FDCP-mix cells cultured under conditions which lead to self-renewal than under conditions which lead to granulocyte-macrophage differentiation. Under the latter conditions, Cl(4)pHQ and Cl(4p)BQ even stimulated growth at intermediate concentration levels. In the primary cell cultures, pronounced differences were observed in the sensitivity between individual developmental pathways and between the different compounds. The percent of cells differentiating into the granulocytic lineage was increased at high concentration levels of each test compound. However, stimulatory effects on the macrophage lineage were observed at intermediate concentration levels of Cl(4)pHQ, Cl(4p)BQ and 2,4,6-Cl(3)P, and differentiation into erythrocytes was stimulated at low concentrations of 2,4,6-Cl(3)P. It is concluded that chlorinated monocyclic pesticides, after biotransformation to quinoid metabolites, may interact directly with haemopoietic progenitor cells with differential effects on self-renewal and differentiation. These mechanisms could lead to myeloplastic disorders.

Association of elevated blood levels of pentachlorophenol (PCP) with cellular and humoral immunodeficiencies.

It has long been suspected that pentachlorophenol (PCP) exerts a damaging influence on the immune system. In this study, the possible relationship between blood levels of PCP and immune function was studied in 190 patients who had been exposed for more than 6 mo to PCP-containing pesticides. The patients suffered from frequent respiratory infections and general fatigue. Lymphocyte subpopulations, in-vitro responses to mitogens, allogeneic stimulator cells, plasma neopterin, cytokines, soluble cytokine receptors, soluble adhesion molecules, and immunoglobulin autoantibodies were determined. A dose-response relationship between blood levels of PCP and cellular and humoral immune parameters was established. Blood levels of PCP were associated negatively with (a) total lymphocyte counts (p = .0002), CD4/CD8 ratios (p = .0015), and absolute counts of CD3+ (p < .0001), CD4+ (p < .0001), CD16+ (p < .0001), CD25+ (p = .0003), DR+ (p < .0001), CD8+/56+ (p = .020), and CD19+ cells (p = .092); (b) plasma levels of interleukin-2 (IL-2) (p < .0001), soluble IL-2R (p < .0001), IL-6 (p < .0001), IL-10 (p = .0039), interferon-gamma (IFN-gamma) (p < .0001), tumor necrosis factor-alpha (TNF-alpha) (p < .0001), transforming-growth factor-beta2 (p = .023), soluble IL-1 receptor antagonist (sIL-1 RA) (p < .0001), soluble intercellular adhesion molecule-1 (p = .0003); and (c) immunoglobulin (Ig) M-anti-Fab type autoantibodies (p = .0353). PCP levels were associated positively with (a) number of impaired stimulation assays per patient (p = .041); (b) number of circulating CD11b+ monocytes (p = .0015); and (c) plasma levels of neopterin (p < .0001), IL-4 (p = .020), and sIL-6R (p = .020). Compared with patients who had PCP plasma levels that were less than or equal to 10 microg/l, patients with blood levels of PCP that exceeded 10 microg/l experienced the following more often: low numbers of total blood lymphocytes (p = .054), CD3+ (p = .0014), CD4+ (p = .0001), DR+ (p = .0003), CD16+ (p = .0033), and CD25+ cells (p = .0033). In addition, the same aforementioned patients experienced the following more frequently: undetectable plasma levels of IL-2 (p = .0057), IL-6 (p = .042), IL-8 (p = .038), IL-10 (p = .0001), TNF-alpha (p = .0062), and IFN-gamma (p = .016); and impaired in-vitro responses of lymphocytes (p = .071). The authors concluded that increased blood levels of PCP were associated significantly with cellular and humoral immunodeficiencies. Recurrent respiratory infections and general fatigue could originate from PCP-associated immunosuppression.

Long-term exposure to wood-preserving chemicals containing pentachlorophenol and lindane is related to neurobehavioral performance in women.

BACKGROUND: The adverse neurobehavioral effects of long-term low exposure to wood-preserving chemicals (WPC) containing solvents, pentachlorophenol (PCP) and gamma-hexachlorocyclohexane (gamma-HCH; lindane), and other neurotoxicants were investigated in a neuropsychological group study. METHODS: Out of a population of 2,000 women visiting the outpatient practice of a gynecological department, a sample of 15 women aged 31-56 (mean 43) with long-term exposure to WPC verified by self-report, biological monitoring, and environmental samples was investigated. Fifteen controls aged 42 (31-56) years were drawn from the same population and pair-wise matched with respect to sex, age, education, and estimated intelligence. RESULTS: For the exposed group, mean PCP serum level was 43.6 micrograms/l and mean gamma-HCH blood level was 0.085 microgram/l. Mean duration of exposure was 10 (5-17) years. Intellectual functioning, attention, memory, and visuo-motor performance were examined, suggesting significant group differences in visual short-term memory (Benton Test; d = 1.5, P = .005), verbal memory (paired associate learning and Peterson paradigm; d = 4.3 and 1.6, P < .001), and an incidental learning task (d = 2.3; P = .001). Frequent subjective complaints as assessed by questionnaire were attenuated motivation (d = 1.7; P = .001), increased fatigue (d = 1.6; P = .001), distractibility (d = 1.0; P = .003), and depressed mood (d = 1.9; P = .004). PCP blood level was significantly associated with paired-associate learning, Benton Test, and reading/naming speed. CONCLUSIONS: Long-term low-dose exposure to WPC in the domestic environment could be related to subjective complaints (attention, mood, and motivation) and to subtle alterations of neurobehavioral performance (e.g., working memory) in women.

Pentachlorophenol exposure in women with gynecological and endocrine dysfunction.

Exposure to wood preservatives containing pentachlorophenol (PCP) was detected in 65 women who consulted the Endocrinological Department of the University Hospital of Obstetrics and Gynecology, Heidelberg, Germany, because of gynecological problems. Blood PCP levels ranged from 20.7 to 133 microg per liter of serum. One hundred and six women with similar clinical conditions, corresponding age and body weight, no PCP exposure in history, and PCP levels below 20 microg per liter of serum served as control group. Significant associations were found between serum PCP concentrations, age, and different parameters of the endocrine system. PCP may act centrally on a hypothalamic or suprahypothalamic level which may result in mild ovarian and adrenal insufficiency. PCP may, therefore, play a role in the increasing infertility problem.

National identity and controversy: New Zealand's clean green image and pentachlorophenol.

In the 1990s regulatory bodies in New Zealand worked to develop guide-lines to clean up the contamination of land caused by the use of pentachlorophenol in the treatment of timber. In contrast, there has been little effort to identify and compensate workers contaminated at these sites. This paper explores some of the reasons why action over the contaminated land was relatively quickly taken, whilst there was a lingering controversy over the health of the workers who used pentachlorophenol. The case study suggests that symbols of national identity can play an important role in the resolution of controversy.