Dose response assessment of silica exposure and poisoning of construction workers

ABSTRACT

Airborne exposure to silica, below statutory industrial standards, can cause silica exposure and poisoning in construction workers at higher rates than predicted. This research aimed to assess the respiratory health of construction workers exposed to silica from tiles, bricks, mortar, and concrete. The study found a positive correlation between construction material dust and fume exposures and workplace seniority. Silica poisoning was dose-dependent on cumulative silica dust or fumes exposure. The average industrial silica particles and emissions BMDLs were 0.68 and 0.30 mg year/m3, respectively. Silica dust and fume BMDLs for silica poisoning were 0.02 mg/m3 and 0.01 mg/m3, respectively. The study concluded that the current exposure levels for silica in China should be re-evaluated, and operational cumulative exposure limits should be established for better prevention of silica poisoning. The study also noted that disparities in sensitivity to silica poisoning may be related to genetic factors and gene-environment interactions.

KEYWORDS:

• Dose response assessment
• dose-effect relationships
• silica exposure
• construction workers

1. Introduction

Silica dust is a complex mixture of particles that may vary in size, shape, and composition depending on the source of the dust. It is also a naturally occurring mineral commonly found in many construction materials such as concrete, bricks, and rocks. One important distinction is between pure silica dust, which consists of 100% crystalline silica particles, and total silica dust, which includes both crystalline and non-crystalline forms of silica. Crystalline silica is the form that is most commonly associated with the development of silicosis and other related diseases, but non-crystalline silica may also pose health risks, particularly if it is inhaled in high concentrations [1]]. Another important factor is the size of the silica particles, which can impact their ability to penetrate the respiratory system and cause damage. Respirable silica dust refers to particles that are small enough to enter the deepest parts of the lungs, where they can cause the most harm [2]. In the construction industry, exposure to respirable crystalline silica dust can lead to the development of silicosis, a potentially fatal lung disease. In some countries, the definition of silica dust may include a requirement for a minimum percentage of crystalline silica content. This can impact how exposure levels are calculated and may lead to differences in reported levels of silica dust across different studies. In recent years, there has been increasing concern about the extent of silica exposure and poisoning among construction workers and the need for better measures to assess and prevent this health risk. There have been several studies that have investigated the relationship between silica exposure and silicosis.

The finding that the dose-response relationship between silica dust and silicosis may be different in various worksites highlights the importance of understanding the specific occupational hazards present in different industries. The higher risk of silicosis in metal mines compared to pottery factories suggests that the type of work, as well as the characteristics of the silica dust exposure, can have a significant impact on disease risk. The 44-year cohort study referenced in the statement provides valuable insight into the long-term effects of silica dust exposure in these two industries. The results of this study can inform public health policies and workplace safety regulations to help prevent occupational silicosis and other related diseases [3]. It is also worth noting that while this study specifically looked at metal mines and pottery factories, other industries may have different dose-response relationships between silica dust and silicosis [1–3]. Therefore, further research is needed to better understand the potential variation in disease risk across different worksites and to develop tailored prevention strategies based on industry-specific hazards.

This paper explores the relationship between the level of silica exposure and the resulting health effects on construction workers. By analyzing data from studies and workers’ health records, we can better understand the impact of silica exposure on workers’ health and identify effective strategies for reducing this risk [4,5]. Past studies indicate a significant correlation between silicosis development and silica exposure dust, indicating that cumulative silica exposure increases the risk of silicosis, with an annual prevalence of silicosis growing massively [6]. The purpose of this study is to investigate the relationship between silica exposure levels and the incidence of silica poisoning in construction workers through a comprehensive dose-response assessment to inform effective preventive measures and improved occupational health and safety standards.

2. Materials and methods

This research applies the meta-analysis technique using the statistical technique to gather data from several credible resources to come up with more accurate information on Silica’s effects when inhaled and exposure risk. This approach is suitable for synthesizing the existing evidence on the effects of interventions, exposures, or risk factors.

2.1 Dose-response assessment

Dose-Response Assessment might influence workplace selection. Massive amounts of particles per cubic foot (mppcf) are used to quantify and determine the current OSHA acceptable exposure level (PEL) for fine particulate matter containing crystalline Silica (SiO₂) in the construction sector [29 CFR × 1926.55]: PEL = % silica+5 and 250 mppcf (porphyria) is one of the porphyrias, a set of illnesses [7]. A series of diseases known collectively as porphyria (por-FEAR-e-uh) are brought on by an accumulation of the body’s natural chemicals that create porphyrin. Haemoglobin, a protein found in red blood cells that forms a bond with porphyrin, binds iron and transports oxygen to the body’s tissues and organs, depends on porphyrins for proper function. Porphyrias are characterized by excessively high amounts of porphyrins and porphyrin precursors in the body due to enzyme deficits required for the formation (synthesis) of heme, a component of haemoglobin. Silica poisoning is the harmful impact of a progressive build-up of Silica in bodily tissues caused by frequent exposure to silica-containing chemicals. Additionally, risk patterns may change depending on which ethnic groups have a higher or lower prevalence of polymorphisms. The idea of genotype pre-employment testing has been put up. But this is currently not feasible. It is difficult to identify a no (NOAEL) or lowest (LOAEL) observable adverse impact threshold because most studies only permit inferences about differences between groups with different exposures [3,6].

Additionally, there have been few subjects that have been revealed at work. On the other hand, impacts may appear at low – slung contact or even at a low frequency when discrete exposure measures are utilized in huge populations. Meanwhile, delicate techniques have been applied. It consequently becomes more challenging to determine if the consequences should be viewed as unfavourable (e.g. presenting health risk problems and serving as a groundwork for risk assessment). In this paper, the correlation between a subject’s estimated dosages based on silica exposure levels has been called, and the strength of a certain impact on the dose connection has been built. However, most effects do not have enough data to represent acceptable dose-effect bends. For some products, it is possible to make educated guesses about where the dose-effect curve might be at various points; and other effects. The no-detected-effect threshold describes this point. The number of studies showing no result and the sample size will determine how confident people can be in such estimates.

2.2 Occupational exposure to silica

Several studies have been conducted to assess the risk of occupational exposure to Silica. The data from these studies have been used to determine the no-detected-effect thresholds (NOAEL) and the lowest-observed-adverse-effect levels (LOAEL). The benchmark concentration limit at a 99% lower confidence limit (BMCL01) was used as the basis for the chronic reference exposure level (REL). The studies are summarized in the table below, showing the outcomes of each research. Table 1 provides a summary of the no-detected-effect thresholds that were discussed. For several of these effects, dose-response relationships can be established. A total of 5 good-quality studies on occupational exposure to Silica have been conducted, summarised in the following tables.

Table 1. Summary of studies considered for risk assessment.

Study	Steenland and Brown,1995	Hughes et al., 1998	Chen et al., 2001	Churchyard et al., 2004	Ehrlich et al., 2018
Population	3330 S. Dakota gold miners	1809 California diatomaceous earth workers	3010 miners in China	510–520 black South African gold miner	2245 white gold miners in South Africa
Population with silicosis	170 miners (5.1% of the population)	81 miners (4.5% of the population)	1015 miners (33.7% of the population)	93 miners (5.6% of the population)	313 miners (14% of the population)
Exposure Route	Inhalation	Inhalation	Inhalation	Inhalation	Inhalation
Exposure duration	8 hours per day 40 hours per week 3–36 years (mean = 9 years)	8 hours per day 40 hours per week 1–45 years (mean = 11.5 years)	8 hours per day 40 hours per week 2.2 years for NOAEL Group	270 shifts/year	8 hours per day 40 hours per week 10–39 years (mean = 24 years)
NOAEL	Not Found	≤1 mg/m^3-years (6 cases)	≤10 mg CTD/m3-years (2 cases) ≤ 360 µg silica/m3 – year	Not identified	2 mg/m^3/years - CDE (without any silicosis)
LOAEL	0–0.2 mg/m^3/years - CDE (5 miners silicosis)	>1, ≤ 3 mg/m^3-years (17 workers with silicosis)	10–19.99 mg CTD/m^3-years (24 cases)	0–0.80 mg/m^3-yr (11 cases)	3 mg/m^3/years - CDE (9 miners silicosis)
BMCL01	0.34 (mg/m^3)–yr	Not Found	132 µg silica/m^3 – years	0.673 (mg/m^3)-yr	2.12 (mg/m^3)–yr CDE or 0.636 (mg/m^3)–yr silica
Averageexperimental exposure	112μg/m^3-yr silica at BMC01 (340 x 10 m^3/20 m^3x 5d/7d x 48wk/52wk) 112μg/m^3-yr/9 yr = 12.4μg/m^3	≤330 µg/m^3-y (1000 x 10/20 x 5/7 x 48wk/52wk) ≤ 330 µg/m^3-y/11.5years = ≤ 29µg/m^3	40 µg/m^3-y (132 x 10/20 x 5/7 x 48wk/52wk) 40 µg/m^3-y/2.2 years = 18 µg/m^3	249 (µg/m^3)-yr (673 x 10/20 x 270 shifts/365) 249 (µg/m^3)-yr/21.8 yr= 11.4µg/m^3	235 μg/m^3-yr silica at BMC01 (636 x 10 m^3/20 m^3x 270 shifts/365 days) 235 μg/m^3-yr/24 yr = 9.8 μg/m^3
Study design	Retrospective cohort study	Retrospective cohort study	Retrospective cohort study	Cross-sectional study	Retrospective cohort study

The above table illustrated diverse research on silica exposure and dose-response in a diverse population with silicosis, their exposure routes, exposure duration, NOAEL, LOAEL, BMCL01, the research design, and their average experimental exposures. The United States Environmental Protection Agency (EPA) selected the research conducted by Hnizdo and colleagues as the reference study. To account for the insensitivity of x-rays in the diagnosis of silicosis and to reduce the possibility of false-negative results, repeated x-ray scans were performed on each miner as part of the ongoing, long-term investigation. These scans were performed to account for the insensitivity of x-rays [8,9]. The classification of silicosis that the International Labor Organization (ILO) considers the one with the least severe symptoms was adopted in the inquiry.

It was discovered that the incidence of silicosis was 1.9% (9/474) with 0.9 mg/m³ yr silica (p = 0.064 by Fisher exact test, two-tailed; 0/204 vs 9/474) [10]. Because this incidence is so near to the limit of the data’s sensitivity and because silicosis is a terrible and irreversible outcome, a BMCL01 was chosen to serve as the basis for the chronic REL. This enormous investigation has a statistical significance that is high enough to pick up on replies with an incidence rate that is lower than 5%.

2.3. NOAEL and LOAEL values

Table 2 summarises the NOAEL and LOAEL doses for silicosis. A concentration of 2 mg/m³-years CDE Silica had no observed detrimental effects on gold miners, while a concentration of 3 mg/m³-years CDE had the lowest reported unfavourable effect level. The Hnizdo and SuisCremer study is the most conservative study for NOAEL and LOAEL compared to previous investigations. In addition, the population’s sample size is more reliable due to the large sample size of up to 2,235 gold miners serving as the study population.

Table 2. Estimation of NOAELs and LOARLs for silicosis.

Study	Subjects	NOAEL in µg/m^3-yr	LOAEL in µg/m^3-yr
Steenland and Brown,1995	3330 S. Dakota gold miners	Not Found	0–0.2 mg/m^3-years
Hughes et al., 1998	1809 California diatomaceous earth workers	≤1 mg/m^3-years	>1, ≤ 3 mg/m^3-years
Chen et al., 2001	3010 Chinese tin miners	≤10 mg CTD/m^3-years ≤ 360 µg Silica/m^3 - years	10–19.99 mg CTD/m^3-years
Churchyard et al., 2004	510–520 black South African gold miners	Not identified	0–0.80 mg/m^3-yr
Ehrlich et al., 2018	2235 white South African gold miners	2 mg/m^3-years CDE	3 mg/m^3-years CDE

2.4. Cumulative exposure silica curve

Using Hnizdo and Sluis-Cremer data, the U.S. Environmental Protection Agency (1996) performed a thorough baseline assessment (Figure 1) [10]. Their technique led them to determine that exposure to 1.31 (mg/m³) yr of Silica dust, the lower limit for a 1% risk of silicosis (BMCL01), is the same as being in continual contact with 6.7 (g/m3) Silica over 70 years. USEPA used neither the BMC/UF nor the NOAEL/UF methods to produce a formal Reference Concentration (RfC) for Silica.

Figure 1. Cumulative Silica risk curves estimated by the EPA.

Five research findings are presented in the cumulative Silica exposure (mg/m³ x years) graph. In the study by [10], the NOAEL was determined to be 2 mg/m³ x years without any silicosis cases, while the BMDL01 was calculated to be 2.12 mg/m³ years. Three cases of silicosis were found to correlate with an exposure limit of 1.0 mg/m years, as indicated by the authors and corresponding to a risk of zero.

Leso et al. [11,12] demonstrated the absence of risk for aggregate Silica exposures<1 mg/m years. Ng and Chan’s study also emphasized the consequences of risk suppositions, exposure three bias, or survivor bias. Although Silica is a carcinogenic substance, its carcinogenic pathway has been described and does not involve genotoxicity.

2.5. New research after EPA’s assessment

Park et al. (2002) conducted a quantitative risk assessment of the start of silicosis amongst Lompoc diatomaceous soil employees using Logistic regression methods (Table 3). A linear relative risk model fits the data best [13]. They predicted an additional lifetime risk of 68–75 radiographic silicosis per thousand employees exposed to 50 g/m³ Silica (cristobalite) over a 45-year job and a lifespan of 85 years [14]. At 1 g/m³ Silica, the extra life hazard of non-cancer lung illness was calculated to be 1.6 per thousand exposed workers. Under this kind of parameters, there would still be a substantial risk if BMC/UF utilized the EPA’s BMCL01 as a reference dosage (RfC= [1.31 (mg/m³) yr]/10 = 0.131 mg/m³) yr) [10].

Table 3. Park et al. (2002) predicted the excess lifetime risk of silicosis.

Silica Concentration (mg/m^3)	45 year cumulative exposure in mg/m^3 year	Radiographic silicosis -all workers	Radiographic silicosis in workers with < 10 mg/m^3 year
0.001	0.045	6.2/1000*	1.6/1000
0.005	0.225	17/1000	7.8/1000
0.01	0.45	26/1000	16/1000
0.02	1.8	39/1000	31/1000
0.05	2.25	68/1000	75/1000
0.1	4.5	100/1000	140/1000
0.2	9	150/1000	260/1000

2.6. Cumulative exposure silica curve

Chen et al. [6] was selected as the reference study for the risk assessment in this report because it was likewise a cohort study but had a bigger sample size and a more conservative estimated BMCL01.

A group of 3010 miners working for at least a year in four Chinese tin mines between 1960 and 1965 [6] found a strong, statistically significant correlation between silicosis development and Silica exposure dust. Diseases related to Silica or tin exposure were not mentioned. All of the cohort members were followed up with until the year 1994 [15]. An occupational exposure matrix for each location, job category, and year was created using historical Chinese total dust (CTD) data.

The CTD data were converted into estimates of respirable crystalline Silica to compare with previous population-based studies of silicosis. Each miner’s employment history was culled from official records. Chinese Roentgen criteria for pneumoconiosis from 1986 were used to get the silicosis diagnosis. The standards categorized silicosis as Stage I-III, corresponding to the ILO arrangement of 1/1 or higher [16,17]. There were a total of 1015 miners (33.7%) who were diagnosed with silicotic silicosis (mean age = 48.3 years, mean time from first exposure = 21.3). In the end, 684 people exposed to tin mines contracted silicosis after their exposure ended (mean = 3.7 years later). Cumulative Silica exposure was found to increase the risk of silicosis significantly.

The annual prevalence of silicosis was shown to increase by 68.7% when workers were exposed to a CTD of 150 mg/m³ ( = 5.4 mg/m³ of respirable crystalline Silica). There was no link between latency and the risk or cumulative dose of silicosis (Figure 2) [18,19]. For 45 people exposed to the occupational exposure threshold of 0.1 mg/m³ respirable crystalline Silica for an extended period (4.5 mg/m³ years Silica), the authors calculated a 55% chance of Silica exposure.

Figure 2. The cumulative risk of silicosis versus cumulative exposure to respirable crystalline Silica [6]. .

The study also stated that despite the differences between it and other studies, a Significant correlation suggests that exposure to 100% respirable crystalline Silica dust at the current permissible exposure limits of 0.1 mg/m3 set by the U.S. Occupational Safety and Health Administration (OSHA) and Mine Safety and Health Administration (MSHA) is not silicosis-preventive. Employees who were only meant to be uncovered to occupational levels of 50–100 g/m³ are nonetheless being confirmed with silicosis at autopsy. Because of this, it has been suggested that the current workplace exposure threshold of 100 g/m³ for inhalable, crystalline Silica (more precisely, alpha-quartz) be reduced to 50 g/m³ [6]. The authors gave some reasons for differences in findings between their study and other studies, such as the duration of follow-up, different diagnostic methods for the detection of silicosis,

3. Results analysis

3.1 Exposure assessment for occupational exposure in construction works

Various construction works produce significant Silica dust, which can cause silicosis. As in the objective of the studies, Silica dust exposure from selected construction work shall be determined and identified. In the study of [6] a total of 8 construction activities were evaluated and analyzed in Table 4:

Table 4. Mean ambient Silica concentrations from work activities identified in a construction site.

Construction Activities	Mean (mg/m^3)	% Quartz Samples < LOD	TLV Exceed %
Clean-up	0.03	36	50
Hand demolition	0–10	7	88
Concrete cutting	0.07	7	77
Concrete mixing	0.02	56	20
Tuck-point grinding	0.22	0	100
Surface grinding	0.63	0	100
Sack and patch concrete	0.03	54	40
Concrete floor sanding	0.07	33	80
Mixed	0.22	0	97

The Silica dust average concentration from each construction activity was measured and monitored as presented above (Table 4). During the assessment, 113 samples were collected and represented eight types of construction activities and one mixed construction activity. An average of 220 minutes are run for the samples. The study’s three highest Silica dust exposure were tuck-point grinding, surface grinding, and mixed construction activities. Varied construction activities generated significant Silica dust, most probably caused by the amount of surface scraping as one part of the activities in the samples [8]. At the same time, the three lowest generations of Silica dust fall under concrete mixing, clean-up and sack and patch concrete.

Comparing the geometric means for Silica dust with the ‘American Conference of Governmental Industrial Hygienists threshold limit value’ (TLV) of 3.0 mg/m³, 34% of the samples exceed the limit [20,21]. Overall the geometric mean quartz run time average was 75% with a concentration of 0.11. Five of the eight activities showed that most results exceeded the quartz TLV. The percentage of the respirable quartz samples in the range of 2.2 to 21.0% is based on the activity.

Studies showed that 4.5-inch mills produce 33% less dust than 7-inch grinders, and abrasive grinding causes 60% less generation of dust exposure. Twenty-three samples were collected to measure the quartz dust concentration, and results showed the average dust exposure concentration with a mean of 0.63 mg/m³ [22]. Results were followed by tuck-point grinding and mixed construction activity with a mean of 0.22 mg/m³. By referring to the BMCL 01 as the benchmark concentration lower boundary, exposure to the top 3 events in construction becomes a significant risk to human health. Surface grinding showed that the orientation of quartz with 3.4 years may have caused silicosis. Followed by tuck-point grinding and mixed construction activities. If the exposure of 9.6 years, the person may affect by silicosis. All three have a higher possibility of silicosis within ten years.

4. Discussion

4.1 Risk analysis

4.1.1. Risk assessment

After obtaining the relevant exposure levels, the following table was constructed for each work activity in construction works. The initial step was to adjust the background levels to be about the same as one would experience during an eight-hour workday [23]. According to EPA dosages evaluation tools, the health risks associated with consistent (24-h) acquaintance to 3 and 8 g/m³ are presumed to be equivalent to those related to 8-h workers exposed to 8.4 and 22.4 g/m³, including The BMCL01 derived from the study by [6] will be used for the reference dose in our risk assessment.

Since BMCL01 = 132 µg silica/m³ – years, taking into account uncertainty factors for pharmacokinetic and pharmacodynamics in humans, the reference dose is RfC =BMC/UF = (132 µg Silica/m³ yr)/10 = 0.0132 mg/m³ yr).

In our risk assessment, we assumed that a construction worker in Singapore will start work at 20 years old, work until retirement age at 67 years old, and live to 91 years old due to increased life expectancy in the future. Workers will be assumed to work five days a week, in 8-hour shifts [24]. Each work activity is assumed to take up 2 to 5 hours in an 8-hour work day.

The relevant conversion formula is as follows:

(Exposure level) x A hr/8 hr x 5 days/7 days x 10 cm³/20 cm³ x 47 yrs = (Cumulative Exposure)

The risk assessment will be repeated with the BMCL₀₁ from Hnizdo and Sluis-Cremer for comparison.

Based on BMCL₀₁, a risk quotient within 1.00 is considered acceptable exposure to the person at work. Due to the risk assessment results, all eight construction activities exceeded the risk quotient limit. The highest risk was surface grinding, which produced significant Silica dust during the 2.43 hours and reached a risk quotient of about 224.63 (Table 5).

Table 5. Risk assessment for construction activities was identified using BMCL₀₁ from [6].

Construction Activities	Mean ambient Silica concentration (mg/m^3)	Duration of task (hrs)	Cumulative exposure (47 years) [(mg/m^3)–yr]	RFC (mg/m^3-yr)	Risk Quotient	Acceptable/Not Acceptable
Clean-up	0.03	3.76	0.218473	0.0132	16.55095	Not acceptable
Hand demolition	0.10	3.58	0.693379	0.0132	52.52872	Not acceptable
Concrete cutting	0.07	4.75	0.64399	0.0132	48.78715	Not acceptable
Concrete mixing	0.02	4.37	0.169277	0.0132	12.82405	Not acceptable
Tuck-point grinding	0.22	2.13	0.907591	0.0132	68.75687	Not acceptable
Surface grinding	0.63	2.43	2.965067	0.0132	224.6263	Not acceptable
Sack and patch concrete	0.03	3.65	0.212081	0.0132	16.06675	Not acceptable
Concrete floor sanding	0.07	3.07	0.416221	0.0132	31.53191	Not acceptable
Mixed	0.22	3.78	1.610654	0.0132	122.0192	Not acceptable

The reading of 122.02 in the risk quotient refers to mixed construction activities, which showed a very significant risk to human health [20]. Even concrete mixing and clean-up activities showed the least risk quotients, about 12.82 and 16.55. But it still much exceeded the limit of the risk quotient. Due to the over limit of the risk quotient issue, the risk assessment was revised and discussed. Theoretically, the study showed a very strong and reliable report on the Silica dust exposure BMCL_01, and it is not reasonable and practicable in actual practice [6].

The second risk assessment, BMCL_01, was used to evaluate and analyze the risk quotient for the eight selected construction activities. The highest risk was still referring to surface grinding, which produced significant Silica dust during the 2.43 hours, and the risk quotient reached 46.62. Compared with the previous reading from [6] study, it is still possible to implement the control measure with the effective measurement of at least 50 times of protective factors. The reading of risk quotient 25.32 refers to mixed construction activities.

Even concrete mixing and clean-up activities showed the least risk quotient, about 2.66 and 3.44. But it still much exceeded the limit of the risk quotient [25]. Risk assessment based on BMCL₀₁ from [26,27] was more reasonable and practicable. The risk quotient can be reduced by implementing safety measurements. Risk can be reduced by wearing respirators. NIOSH-approved N95 respirators, such as the the8210 and 8110S manufactured by 3 M Company, are intended to reduce the wearer’s exposure to specific airborne particles between 0.1 and>10.0 microns in size.

4.1.2. Risk characterization

The hazards of Silica were identified, which are mainly due to silicosis and its associated conditions. Silica enters the human through inhalation of dust, and entry into the lower respiratory tract depends on the particle size spread.

While there are various mechanisms to remove Silica from the lungs, above a threshold amount inhaled, Silica stays in the lungs as it destroys the macrophages that engulf it. Silicosis was the main outcome studied in this project. Available epidemiological and clinical data have been identified, focusing on human data to remove uncertainties of interspecies differences.

The dominant route of exposure was through inhalation since the risk of developing silicosis depends on cumulative Silica dose. Therefore, since Silica has minimal absorption, the following pharmacokinetic parameters of distribution, metabolism and excretion have little relevance to the main outcome of silicosis. With this in mind, the dose-response curve focused on the interaction between the risk of developing silicosis and the cumulative Silica dose a human is exposed to.

Our approach is not without limitations. No comparisons between the risks of silicosis for healthy subjects and smokers or those with lung disease were made due to the lack of clear evidence of smoking or respiratory conditions potentiating the risk of silicosis between the different groups. Our exposure assessment did not differentiate between activities done in enclosed spaces and outdoors, affecting the concentration of ambient Silica-containing dust. As can be seen from the large risk quotients generated, our risk assessment outcomes are vastly different from previous assessments. Still, we believe it is because we chose a far more conservative approach, and excess safety comes at the price of feasibility. However, we believe that our results show that silicosis persists as an occupational disease, not because of unsafe practices alone but also due to its inherent hazardous nature. Besides, it is important to carefully consider the definitions and methods used in different studies when comparing findings related to silica dust exposure and health outcomes. This can help to ensure that the results are accurately interpreted and applied to efforts aimed at preventing or reducing occupational exposure to silica dust.

5. Conclusion

In summary, the study conducted two risk assessments using BMCL01 to evaluate the risk quotient for eight selected construction activities. The exposure assessment identified work activities in the construction industry. Exposure scenarios for construction workers were accessed based on ambient Silica emissions from various work activities and time spent exposed to silica-containing dust. The results showed that all activities exceeded the risk quotient limit, with surface grinding producing the highest risk quotient of 46.62. The second risk assessment was more reasonable and practicable, and it was found that the risk quotient could be reduced by implementing safety measures such as wearing respirators. The hazards of Silica were identified as mainly due to silicosis and its associated conditions, and the dominant route of exposure was through inhalation. The dose-response curve focused on the interaction between the risk of developing silicosis and the cumulative Silica dose a human is exposed to. The overall picture of risk gleaned is that if risks of developing silicosis were accessed with a very conservative reference concentration in our case, most current emissions are likely to be deemed as hazardous due to the large risk quotient generated from prolonged work on a timescale of years. An approach to finding a reference concentration that will ensure low risks of silicosis (<1%) ultimately proved unpractical. However, the results indicate that silicosis continues to be an occupational disease not just due to unsafe practices but also due to its hazardous nature. One of the identified limitations includes the lack of comparison between the risks of silicosis for healthy subjects and smokers or those with lung disease and not differentiating between activities done in enclosed spaces and outdoors. Therefore, more research on the subject is recommended to compare these risks.

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Additional information

Funding

This research was funded by Enerstay Sustainability Pte Ltd (Singapore) Grant Call (Call 1/2022) _SUST (Project ID CAA-2003), Singapore.