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Article

Exposure to Lead Compounds in an Industrial Setting and the Effects on the Thyroid Gland: A Pilot Cohort Study

by
Lidia Caporossi
1,*,
Simona Di Renzi
1,
Mariangela De Rosa
1,
Silvia Capanna
1,
Elisa Partenzi
1,
Iacopo D’Alessandro
2 and
Bruno Papaleo
1
1
Department of Occupational and Environmental Medicine Epidemiology and Hygiene, National Institute for Insurance Against Accidents at Work, 00078 Monte Porzio Catone, RM, Italy
2
Centro Sicurezza Lavoro, 00040 Pavona, RM, Italy
*
Author to whom correspondence should be addressed.
Hygiene 2025, 5(2), 13; https://doi.org/10.3390/hygiene5020013
Submission received: 25 February 2025 / Revised: 26 March 2025 / Accepted: 1 April 2025 / Published: 3 April 2025
(This article belongs to the Section Occupational Hygiene)
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Abstract

:
Background: Lead compounds are chemicals of high toxicological concern and are suspected to interact with the thyroid axis. Method: A cohort study was carried out involving 70 workers from a petrochemical company exposed to inorganic lead compounds. All recruited workers were given a clinical anamnestic questionnaire aimed at characterizing their endocrine and thyroid status. A blood test was conducted to dose the amount of lead, thyroid hormones (FT3, FT4, TSH), and antibodies (TGAb and TPOAb). Samples were stratified according to working seniority and lead exposure levels. A regression study was conducted to highlight trends in hormones and antibodies versus lead levels. Results: Most of the dosages are within the normal ranges. The regression study showed how higher lead values are correlated with a reduction in TSH and an increase in FT3 and FT4. There is a statistically significant increase in TPOAb in the most exposed workers. Conclusions: The trends of thyroid hormones may suggest a tendency towards hyperthyroidism for higher lead exposure, while the increase in TPOAb could indicate a greater predisposition to the development of autoimmune thyroid diseases.

1. Introduction

Lead is one of the most widely used heavy metals, with extensive applications dating back to ancient times [1]. In nature, lead is not found in its elementary form but primarily exists in its divalent state, forming inorganic compounds, or in its tetravalent state, which gives rise to a wide range of organic compounds.
In developing countries, lead pollution remains a significant public health concern [2,3,4]. To mitigate exposure among workers and the general population, numerous regulatory restrictions have been implemented in Europe. Nevertheless, lead and its compounds continue to be essential industrial chemicals used worldwide. Notably, lead ranks as the fifth most important metal in terms of production and application, with over ten million tons produced annually in Europe [5].
Existing literature suggests that exposure to lead compounds in daily life primarily occurs through ingestion, with estimated intake levels ranging between 200 and 500 µg/die [6]. In occupational settings, however, inhalation of lead-containing fumes or dust represents the primary route of exposure. Approximately 35% of inhaled lead reaches the bloodstream, and through it, lead is subsequently distributed to soft tissues and bones. A portion of the absorbed lead is excreted directly through urine [7].
Workers may be exposed to lead in both mineral and organic forms. Mineral compounds are primarily absorbed through the lungs and the gastrointestinal tract, whereas organic compounds are absorbed through the skin [8]. The severity and duration of adverse effects associated with lead exposure depend on both the concentration and the length of exposure. The international Agency for Research on Cancer (IARC) has classified metallic lead and its inorganic derivatives as Group 2 of carcinogens [9].
Lead can be found in different industrial production, including battery manufacturing, ceramics, rubber production, lead bullets, ammunition, and protective barriers against ionizing radiation.
Historically, industrial workers have been extensively exposed to lead, with documented cases of hematological, gastrointestinal, rheumatological, endocrine, neurological, and renal disorders. As a result, lead is considered one of the most hazardous environmental pollutants [1]. Occupations with the highest levels of lead exposure include those in the petrochemical industries, rechargeable battery manufacturing, and munitions production. Specific lead compounds, such as oxides, carbonates and chromates are used as pigments in the glass, ceramics, and paint industries [10]. Additionally, certain lead salts are incorporated into plastic materials. In the past, organic lead compounds were commonly used as antiknock agents in fuel; however, regulatory restrictions have been implemented in Europe to limit their availability.
Prolonged occupational exposure to lead compounds can result in chronic toxicity, a progressive condition with a wide range of symptoms, including arthralgia, headache, weakness, depression, loss of libido, impotence, and gastrointestinal disturbances. Long-term effects may include toxicity for reproduction, chronic renal failure, hypertension, gout, and chronic encephalopathy [11].
During chronic exposure, lead accumulates at the highest concentrations initially in the bones and subsequently in the kidneys. According to the U.S. Centres for Disease Control and Prevention (CDC) and the World Health Organization (WHO), a blood lead level of 10 µg/dL is considered a cause for concern. However, research [11] indicates that lead exposure can result in developmental impairments and adverse health effects even at lower concentrations.
Several studies [12,13] have suggested that lead compounds may pose a significant risk to the endocrine system. In particular, inorganic lead compounds have been shown reprotoxic effects, affecting both male and female reproductive systems [14,15]. Additionally, lead exposure during pregnancy has been associated with adverse fetal outcomes [16,17].
Focusing on the effects of lead exposure on thyroid function, several studies have highlighted its potential harm to workers and have provided evidence suggesting a detrimental impact on the thyroid, including an increased risk of hypothyroidism, despite some existing controversies [18,19].
The potential effects of lead on thyroid function have been a subject of investigation for over fifty years. One of the earliest studies by Slingerland et al. [20] demonstrated reduced iodine uptake by the thyroid gland in cases of high lead exposure. These findings were later confirmed in both rat models and in vivo studies by Sandstead et al. [21]. Some authors have suggested that lead exposure affects both peripheral thyroid hormone levels and thyroid stimulating hormone (TSH) levels [22]. Lead may exert neurotoxic effects on the development of cerebrum and cerebellum through thyroid dysfunction, ultimately leading to increase neurotoxicity [17]. Furthermore, substantial lead exposure has been documented to influence endocrine gland function. Specifically, lead appears to disrupt the hypothalamic–pituitary axis, leading to reduced secretion of TSH, growth hormone (GH), and follicle-stimulating hormone/luteinizing hormone (FSH/LH) in response to thyrotropin-releasing hormone (TRH), growth hormone-releasing hormone (GHRH), and gonadotropin-releasing hormone (GnRH) stimulation, respectively [19].
Initially, lead exposure may result in subclinical testicular damage, followed by hypothalamic or pituitary dysfunction with prolonged exposure [7,19]. In females, lead accumulates in the granulosa cells of the ovary, delaying ovarian growth and pubertal development while also reducing fertility [19].
According to a study [23], lead exposure can lead to functional deterioration of the pituitary–thyroid axis, modifying the thyroid physiology. Chronic lead exposure has also been associated with anatomic–histological changes in the thyroid gland, including a reduction in thyroid follicle size and nuclear alterations in follicular cells [22]. Recent studies [24] have further highlighted the impact of lead on thyroid function, demonstrating reduced production of tetraiodothyronine (T4) and increased secretion of TSH [25]. Additionally, some findings suggest that lead exposure may increase the risk to develop thyroid cancer [26]. Most of these studies [18,24,25] have linked lead exposure to thyroid disfunction and hypothyroidism, particularly in individuals with occupational exposure to this metal. However, further research is needed to confirm these associations and elucidates the underlying mechanisms.
Lead may contribute to the development of both benign and malignant thyroid nodules, affecting thyroid function [25]. Some studies [26] have reported an association between lead exposure and thyroid nodules, particularly in women. However, further research is needed to better understand the relationship between lead contamination and the occurrence of nodular goiter.
In Europe, a specific regulation exists to protect workers from lead exposure, requiring mandatory monitoring of both environmental levels and biological exposure levels. Current biological exposure limits are set at 60 µg/dL of blood for men and 40 µg/dL of blood for women of childbearing age. However, a recent European directive (Dir. (UE) 2024/869) mandates a gradual reduction in these limits in the coming years, lowering the threshold to 15 µg/dL of blood, with an alert level of 7 µg/dL in blood for women.
The management of lead compounds in the workplaces and the worker protection measures are currently regulated by the European legislation, as outlined in Directive (Dir. (EU) 2022/431). This directive requires highly precautionary management of lead, similar to carcinogenic and mutagenic substances, due to its reprotoxic properties.
Figure 1 presents a schematic overview of the main environmental risk factors for thyroid health, which should be considered as possible confounding factors when evaluating exposure to lead compounds. It is important to acknowledge that genetic predisposition plays a significant role in certain thyroid disorders, alongside the higher global prevalence of thyroid disease among women. Additionally, pre-existing autoimmune diseases, such as celiac disease, may represent a risk factor for the development of autoimmune thyroid disorders.
The aim of the present study is to clarify the possible effect of lead exposure to the thyroid gland, focusing on a cohort of industrial workers and their working and pathological history.

2. Materials and Methods

2.1. Population Under Study

This epidemiological study was designed as a cohort study focusing on occupational settings with potential lead exposure. Workers were enrolled after receiving a detailed presentation of the study by the researchers, providing a signed informed consent, and completing a structured questionnaire. The study was conducted according with the Helsinki declaration and was approved by the territorial ethics committee Lazio Area 2; the reference code is 10.23 CET2 asl_rm6.
The study population consisted of individuals employed in the industrial sector, specifically within a petrochemical industry located in Sardinia (Italy), mainly engaged in metal carpentry, connected with the maintenance of mechanical and electrical systems and the welding and cutting of metallic parts. Recruitment was carried out between September 2023 and March 2024.
Participants were selected based on the following eligibility criteria:
(1)
Male or female workers;
(2)
Aged between 18 and 67 years;
(3)
Occupational exposure to lead, with at least one blood lead analysis conducted in the past year;
(4)
No history of thyroidectomy;
(5)
No use of drugs that could replace thyroid hormones;
(6)
Ability to participate in the study (e.g., adequate understanding of the Italian language and normal cognitive function).
A total of 72 workers met the inclusion criteria of occupational lead exposure. However, only 2 participants were women, with less than 4 years of working experience. For the sake of homogeneity of the data, it was decided to exclude them from the study, bringing the sample to 70 men. Additionally, two workers were excluded due to pre-existing thyroid pathologies requiring long-term pharmaceutical treatment with thyroid hormonal therapy. Specifically, one worker (with 30 years of work experience) had been diagnosed with Hashimoto’s thyroiditis, while another one (with 35 years of work experience) has chronic thyroiditis.
Therefore, a total of 68 subjects met all the predefined eligibility criteria.
Each enrolled worker completed a detailed clinical and anamnestic questionnaire and provided a blood sample for the analytical determination of blood lead levels, which was conducted by the factory’s occupational physician. Blood samples were then sent to the laboratory for hormonal and antibody dosage.

2.2. Analytical Methods

Each blood sample was collected in 10 mL vacutainer EDTA tubes, then stored at 4 °C at the local site of sampling before being sent to the laboratory. The blood samples were centrifuged for 5 min at 2400 rpm, and the plasma fraction was separated and stored at −20 degrees before analysis.
The study was made through the ELISA (enzyme-linked-immunosorbent assay) using the Spark® multimode microplate reader (Tecan Group Ltd., Männedorf, Switzerland) and the Immunowash Microplate Washer (Bio-Rad Laboratories srl, Segrate, Milan, Italy). Commercial kits were used to identify free triiodothyronine (FT3), free thyroxine (FT4), TSH, (purchased by DBC—Diagnostic Biochem Canada Inc., London, ON, Canada) thyroglobulin antibody (TGAb) and thyroid peroxidase antibody (TPOAb) (purchased by Orgentec Diagnostika Gmbh, Mainz, Germany). The normal ranges of each parameter for the general population are reported in Table 1, together with the performance parameters of the used kits.
The blood lead values were determined using an atomic absorption equipped with a graphite furnace (GFAAS) (Agilent Technologies, Santa Clara, CA, USA) following the now consolidated analytical procedures for conducting biological monitoring of those exposed to lead [30].

2.3. Statistical Analysis

Statistical analyses on the questionnaire and laboratory data were conducted with SPSS® 25 software (IBM, Armonk, NY, USA) using different techniques depending on the information obtained and the assumptions of the study. A descriptive analysis of the sample studied was initially conducted. The lead exposure data were represented by means and standard deviations, as were the thyroid hormone and antibody data. The values do not follow a normal trend, so the tests used are non-parametric. Specifically, Mann–Whitney U tests, with a significance of 0.05, were performed to study the trend of thyroid hormone and thyroid antibody values between lead exposure groups. Chi-squared tests were applied to highlight any differences between out-of-range values of hormones or thyroid antibodies and lead exposure classes. Regression studies were then conducted between thyroid monitoring values and lead exposure. Special attention was given to seniority, and the tests described above were also conducted for seniority classes (Mann–Whitney and chi-squared test).

3. Results

The descriptive analysis of the sample of population (68 male workers exposed to lead) is reported in Table 2.
Quantitative data are represented through averages and range values, while qualitative data are represented in the form of a percentage value.
Table 3 shows data of thyroid hormones and antibodies and blood lead with average levels and standard deviation. The table also shows information about the percentage of subjects out of the range of normality (for the thyroid hormones and antibodies), being higher than 15 µg/dL or 60 µg/dL of lead in the blood.
The threshold value used to define out-of-range blood lead levels for the male population is currently set at 60 µg/dL, within which all exposed workers in this study fall.
However, the new European Directive 869/2024 mandates a progressive reduction in this limit, lowering it to 30 µg/dL by 2028 and further reducing it to 15 µg/dL thereafter. Consequently, Table 3 also reports the percentage of subjects exceeding these revised thresholds.
Statistical analyses conducted on the study sample were based on the new limit value of 15 µg/dL.
Overall, the findings indicate a reassuring scenario, with most values within the normal ranges. Approximately 10% of workers exhibited elevated antibody levels, while abnormalities in thyroid hormone levels were observed as follows: thyroid-stimulating hormone (TSH) was outside the normal range in just over 10% of subjects, free triiodothyronine (FT3) in approximately 28%.
Notably, if the biological occupational exposure limit of 15 µg/dL was already applied, a substantial part of the study population of workers (nearly 70%) would be classified as exceeding the permitted exposure level.
Thyroid hormone and antibody values were analyzed according to the level of lead exposure (< or >15 µg/dL) and the results of the applied statistical tests are presented in Table 4.
A significant difference was observed in FT4 levels (p = 0.044) between subjects with lead exposure above and below 15 µg/dL, although overall values remained within the normal range. Similarly, a significant increase in TPOAb (p = 0.042) was detected in individuals with higher lead exposure.
Clinically, elevated TPOAb levels indicate an increased predisposition to autoimmune diseases. When markedly above the normal range, they may be indicative of an ongoing autoimmune condition, such as Hashimoto’s thyroiditis. In our study population, 6.2% of subjects exhibited TPOAb levels above the normal range, while 1.8% had borderline values. Notably, these elevated levels were significantly more frequent in individuals with higher occupational lead exposure.
Regarding TSH levels, it is important to note that mean values were considerably lower among workers with greater exposure, a trend also observed in the linear regression analysis, though without reaching statistical significance. The Mann–Whitney U test yielded a p-value of 0.061, which is close to the significance threshold, suggesting that a larger sample size may provide a clearer confirmation of this trend.
Additionally, a chi-squared test was performed to assess potential differences in the prevalence of out-of-range hormone and antibody values across lead exposure categories; however, no statistically significant associations were identified.
Thyroid hormone and antibody values were analyzed with the Mann–Whitney U test according to the working seniority class (< or >20 years). No statistically significant differences emerged; the results are presented in Table 5.
However, among workers with greater seniority, 50% exhibited one or more parameters outside the normal range.
Chi-squared tests were performed to assess potential associations between out-of-range thyroid hormones and antibodies values and both seniority class and lead exposure levels. However, none of these analyses revealed statistically significant differences.
Subsequent regression analyses were conducted to examine the relationship between lead exposure levels and each thyroid hormone and antibody value. The results are shown in Figure 2 and Figure 3, where normal reference ranges have been highlighted to facilitate interpretation.
Each graph displays the respective regression lines along with the coefficient of determination (R2).
Although the results do not reach statistical significance, an inverse correlation trend between blood lead levels and TSH values emerges, potentially indicating an effect on thyroid function. Overall, the observed hormonal trends suggest that as lead exposure increases, FT3 and FT4 levels tend to rise, while TSH levels decrease. From a clinical perspective, these findings could indicate a predisposition toward hyperthyroidism under conditions of higher lead exposure.
TGAb findings are not only exclusive to Hashimoto’s thyroiditis but are also present in other thyroid disorders, such as Graves’ disease. The presence of these antibodies is crucial for accurately assessing thyroid function, and their measurement is commonly used in the follow-up of patients with differentiated thyroid carcinoma, in conjunction with thyroglobulin levels. In our study population, no significant increase in TGAb was observed in relation to lead exposure, likely due to the absence of subjects with diagnosed thyroid disorders. Less than 10% of participants exhibited elevated antibody levels, but these were not correlated with lead exposure.
Regarding TPOAb, regression analysis confirms an increasing trend in antibody levels with higher lead exposure, consistent with the findings from the comparison between individuals with low and high lead exposure.

4. Discussion and Conclusions

The hypothalamic–pituitary–thyroid axis appears to be affected by lead exposure; however, the specific adverse effects of lead on thyrotropic cells remain inconclusive in the literature [19]. Occupational exposure to inorganic lead compounds has been associated with impaired iodine uptake and morphological alterations in thyroid tissue [31].
Findings from in vivo studies remain contradictory. Some studies have reported that the administration of lead compounds to animals results in decreased serum FT3 levels, while other thyroid hormone levels remain unaffected [32,33]. However, these findings have not been consistently confirmed by other researchers [34]. Yousif et al. [23] observed structural changes in the follicular cells of thyroid tissue in rats exposed to lead compounds, suggesting an inhibitory effect on thyroid hormone production.
Some authors have reported a reduced TSH response to thyrotropin-releasing hormone (TRH) in children exposed to lead, as well as in in vitro experimental studies on rats [35]. Our findings are consistent with this hypothesis. However, the literature remains conflicting regarding the role of lead exposure in thyroid hormone imbalance.
In a cross-sectional study, Robins et al. [36] observed a negative correlation between serum FT4 levels and lead concentrations, while TSH and FT3 levels remained within the normal range. Similarly, Dundar et al. [22] reported a negative regression between lead exposure and FT4 concentrations in workers with longer occupational exposure, without significant changes in TSH and FT3 levels.
A study by Tuppurainen et al. [37] on a population of workers with prolonged and intense lead exposure found a negative correlation between exposure duration and FT4 levels, suggesting that long-term lead exposure may suppress thyroid function. However, other studies did not confirm these findings. Schumacher et al. [38] and Erfurth et al. [39] did not identify a significant decrease in thyroid function associated with lead exposure.
Furthermore, occupational lead exposure ranging from 40 to 80 µg/dL was associated with a significant increase in TSH levels, despite normal FT3 and FT4 concentrations [1,40]. On the other hand, Krieg et al. [41] found a significant decrease in total T4 concentrations among individuals exposed to lead, but only in female populations; this effect was not observed in males, consistent with our study findings.
A recent study on the general female population [42] (n = 309) found no alterations in hormone levels but identified a significant correlation between lead exposure (ranging from 8 to 16 µg/dL) and both the prevalence and size of thyroid nodules. Women with higher lead exposure showed significantly increased odds of developing thyroid nodules (OR 2.75, 95% CI: 1.60–4.70).
Similarly, an epidemiological study reported that serum lead levels were approximately six times higher in hyperthyroid patients compared to healthy individuals and twice as high in hypothyroid patients [43], findings that align with our results. A previous study on a female population identified a direct association between lead exposure and TPOAb levels [44], while Abdelouahab N [45] observed an inverse association between TSH levels and lead exposure, consistent with our findings.
However, other cohort studies conducted in occupational settings have reported different trends. For example, in a study of 58 gas station workers exposed to mean lead levels of 90 µg/dL, a direct association between lead exposure and TSH levels was observed [46], with similar findings reported by Sherif et al. [47].
It is important to note that large epidemiological studies on the general population exposed to overall low levels of lead (average 10 µg/dL) have not identified significant correlations between lead exposure and TSH, FT3, or FT4 levels [48,49,50].
Overall, these findings suggest that lead exposure influences thyroid hormone kinetics; however, the specific pattern of this effect remains inconclusive.
Various health agencies have established threshold limit values for lead exposure in the general population. For instance, the Centers for Disease Control and Prevention (CDC) [51] defined a blood lead level of 10 µg/dL as a threshold associated with adverse health effects, including renal tubular damage, neurophysiological and neurocognitive impairments, as well as hearing and growth disorders [52,53,54]. However, the specific blood lead level at which thyroid dysfunction occurs has not been precisely determined.
Some evidence suggests that endocrine alterations may be observed even at low lead concentrations, as reported by several authors [55,56]. However, the clinical significance of these findings, particularly in cases of long-term exposure, remains unclear.
The discrepancy between the various outcomes of the studies could also be linked to the different exposure levels considered, which can be very different between living and working environments, as well as between different work environments.
Although this study was conducted on a relatively small sample, the findings suggest a potential association between lead exposure and thyroid dysfunction, particularly a reduction in TSH levels accompanied by an increase in FT3 and FT4 levels. This trend appears to be more pronounced for FT4, for which statistical significance was observed in the comparison between workers with blood lead levels below and above 15 µg/dL.
The analysis of antibody levels revealed a significant association between TPOAb levels and lead exposure, with antibody concentrations increasing as exposure levels rose. This finding suggests a potential predisposition to the development of autoimmune diseases.
This observation is particularly noteworthy considering that the two subjects excluded from the study, both with 30–35 years of occupational seniority, had been diagnosed with autoimmune thyroid diseases.
However, several confounding factors must be considered, as they may influence the observed potential adverse health effects. These include gender, genetic background, diet, lifestyle, and exposure to other environmental pollutants.
In conclusion, the exposure data do not appear to be alarming at the monitored exposure levels, as most clinical measurements remained within normal ranges. Nevertheless, the correlation between lead exposure levels and the overall trend in hormone concentrations suggests a potential involvement of the hypothalamic–pituitary axis in the effects of lead exposure. These findings highlight the need for further targeted and robust investigations to clarify this potential relationship.

Author Contributions

Conceptualization, L.C.; methodology, L.C., S.D.R., and M.D.R.; software, S.C. and E.P.; formal analysis, L.C. and S.C.; investigation, I.D. and B.P.; data curation, L.C., S.D.R., and M.D.R.; writing—original draft preparation, L.C., E.P., and S.C.; writing—review and editing, L.C. and B.P.; visualization: S.D.R., M.D.R., and I.D.; project administration, L.C. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved by the territorial ethics committee Lazio Area 2 (the reference code is 10.23 CET2 asl_rm6) on 7 September 2023.

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
FT3free triiodothyronine
FT4free thyroxine
TSHthyroid-stimulating hormone
TGAbthyroglobulin antibody
TPOAbthyroid peroxidase antibody
GHgrowth hormone
FSHfollicle-stimulating hormone
TRHthyrotropin-releasing hormone
LHluteinizing hormone
GHRHgrowth hormone-releasing hormone
GnRHgonadotropin-releasing hormone
ELISAenzyme-linked-immunosorbent-assay
EDTAethylenediaminetetraacetic acid.
LODlimit of detection
GFAASgraphite furnace atomic absorption spectrometer
BMIbody mass index

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Figure 1. The main environmental risk factors for thyroid diseases [27,28,29].
Figure 1. The main environmental risk factors for thyroid diseases [27,28,29].
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Figure 2. Thyroid hormones (pg/mL for FT3 and FT4; µLU/mL for TSH) trend with blood lead values (µg/dL of blood).
Figure 2. Thyroid hormones (pg/mL for FT3 and FT4; µLU/mL for TSH) trend with blood lead values (µg/dL of blood).
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Figure 3. Thyroid antibodies (UI/mL) trend with blood lead values (µg/dL of blood).
Figure 3. Thyroid antibodies (UI/mL) trend with blood lead values (µg/dL of blood).
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Table 1. The normal ranges of thyroid hormones and antibodies and performance parameters of ELISA kit.
Table 1. The normal ranges of thyroid hormones and antibodies and performance parameters of ELISA kit.
FT3 (pg/mL)FT4 (pg/mL)TSH (µlU/mL)TGAb (IU/mL)TPOAb (IU/mL)
Normal range2.2–5.3 7.0–22.0 0.3–5.0<100<50
Borderline 100–15050–75
Positive >150>75
Precision intraday 19.7 4.9 7.72.61.6
Precision interday 18.6 11.5 12.35.73.1
LOD 20.3 1.0 0.1105
LOQ 30.6 2.0 0.23015
1 Data at concentration level near to the highest value of normal range; 2 LOD—limit of detection; 3 LOQ—limit of quantification.
Table 2. Descriptive analysis of population.
Table 2. Descriptive analysis of population.
CharacteristicsMales (68)
Age (range)55.82 (25–66)
BMI(%)
Normal39.7
Overweight38.2
First degree obesity14.7
Second grade obesity2.9
Unknown4.4
Actual smokers (%)26.5
Previously smokers (%)30.9
Alcohol consumption (%)
Daily11.8
Weekly4.4
Occasional52.9
Never22.1
Missing8.8
Working seniority (years) and range22.58 (3–40)
Working seniority class (%)
≤20 years33.8
>20 years50.0
Missing16.2
Table 3. Levels of thyroid hormones, antibodies, and blood lead in 68 male workers.
Table 3. Levels of thyroid hormones, antibodies, and blood lead in 68 male workers.
FT3
(pg/mL)		FT4
(pg/mL)		TSH
(µLU/mL)		TGAb
(IU/mL)		TPOAb
(IU/mL)		Pb
(µg/dL)
Average ± SD2.76 ± 1.1417.28 ± 2.751.92 ± 1.7872.33 ± 137.7613.14 ± 29.04 20.47 ± 7.07
Out of range27.9% 0.0% 13.2% 13.2% 5.9% >15 µg/dL 69.1%
>60 µg/dL0.0%
Table 4. Thyroid hormones and antibody levels in the two lead exposure groups (average ± SD).
Table 4. Thyroid hormones and antibody levels in the two lead exposure groups (average ± SD).
UnitExposure LevelMann–Whitney Test
≤15 µg/dL>15 µg/dLp Value
FT3 pg/mL 2.56 ± 1.152.84 ± 1.1330.550
FT4 pg/mL 15.80 ± 3.9317.94 ± 1.680.044 *
TSH µLU/mL 2.68 ± 2.421.59 ± 1.300.061
TGAb IU/mL 110.95 ± 205.5455.07 ± 91.030.770
TPOAb IU/mL 12.94 ± 20.5213.22 ± 32.330.42 *
* Significant value.
Table 5. Thyroid hormones and antibody levels in the two working seniority class (average ± SD).
Table 5. Thyroid hormones and antibody levels in the two working seniority class (average ± SD).
UnitWorking Seniority ClassMann–Whitney Test
≤20>20p Value
FT3 pg/mL 2.60 ± 0.992.90 ± 1.230.897
FT4 pg/mL 17.18 ± 2.7517.50 ± 2.610.678
TSH µLU/mL 1.92 ± 1.441.85 ± 1.890.765
TGAb IU/mL 104.31 ± 187.2552.80 ± 93.320.793
TPOAb IU/mL 10.49 ± 19.8812.12 ± 28.120.718
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Caporossi, L.; Di Renzi, S.; De Rosa, M.; Capanna, S.; Partenzi, E.; D’Alessandro, I.; Papaleo, B. Exposure to Lead Compounds in an Industrial Setting and the Effects on the Thyroid Gland: A Pilot Cohort Study. Hygiene 2025, 5, 13. https://doi.org/10.3390/hygiene5020013

AMA Style

Caporossi L, Di Renzi S, De Rosa M, Capanna S, Partenzi E, D’Alessandro I, Papaleo B. Exposure to Lead Compounds in an Industrial Setting and the Effects on the Thyroid Gland: A Pilot Cohort Study. Hygiene. 2025; 5(2):13. https://doi.org/10.3390/hygiene5020013

Chicago/Turabian Style

Caporossi, Lidia, Simona Di Renzi, Mariangela De Rosa, Silvia Capanna, Elisa Partenzi, Iacopo D’Alessandro, and Bruno Papaleo. 2025. "Exposure to Lead Compounds in an Industrial Setting and the Effects on the Thyroid Gland: A Pilot Cohort Study" Hygiene 5, no. 2: 13. https://doi.org/10.3390/hygiene5020013

APA Style

Caporossi, L., Di Renzi, S., De Rosa, M., Capanna, S., Partenzi, E., D’Alessandro, I., & Papaleo, B. (2025). Exposure to Lead Compounds in an Industrial Setting and the Effects on the Thyroid Gland: A Pilot Cohort Study. Hygiene, 5(2), 13. https://doi.org/10.3390/hygiene5020013

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