Personal exposure to polyaromatic hydrocarbon and inhalation risk assessment among asphalt hot mixed plant and road paving workers

doi:10.21203/rs.3.rs-3406590/v1

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Personal exposure to polyaromatic hydrocarbon and inhalation risk assessment among asphalt hot mixed plant and road paving workers

https://doi.org/10.21203/rs.3.rs-3406590/v1

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Workers exposed to heated asphalt at paving and hot mixed plant jobs may experience fumes and vapours containing hazardous chemicals, including polycyclic aromatic compounds (PAHs), causing respiratory irritation, carcinogenic and non-carcinogenic risk. The study estimated inhalation exposure to PAHs among asphalt workers in hot mixing plants and road paving areas using XAD-2 sorbent tubes and PTFE filter paper. A total ninety-one personal air samples (paving 37 and plant 54) were collected from the worker’s breathing zone. Results were analysed using HPLC, following the NIOSH-5506 method. It was found that the total PAHs (TPAHs) concentration range (composed vapour and particulate phases) was between 0.02-184.71 µg/m³ (mean 21.07 ± 37.36 µg/m³) and the concentration of TPAHs among road paving workers was significantly higher (p 0.05) than the hot mix asphalt plant workers. Among the individual PAHs compound, the mean concentration of Benzo[ghi]perylene (BghiP) was 7.15 ± 17.05 µg/m³ and it was the highest observation value, followed by Benzo[α]Pyrene (BaP) with a mean concentration 3.28 ± 8.46µg/m³, and the exposure level of BghiP and BaP among the paving workers was significantly (p 0.05) higher compared with the plant workers. Health risk assessment suggested increased chances of developing cancer (3.44 x10^− 09 to 3.47 x10^− 04) in the study area, whereas non-cancer hazard quotients and indexes had values of BaP was 8.095x10⁰², which implied that these contaminants have adverse effects on health. The results of our study demonstrate that the asphalt workers are exposed to PAHs and their derivatives constantly at their work sites, and since PAHs are considered non-threshold carcinogens, our observed levels may still be harmful.

Asphalt

road paving

PAHs exposure

inhalation

risk assessment

Bitumen (liquid asphalt) is formed as a byproduct of crude oil distillation and consists of cyclic alkanes, heterocyclic compounds containing nitrogen, oxygen, and sulphur, aromatic hydrocarbons, aliphatic compounds, volatile organic compounds (VOCs), metals, and PAHs, including BaP, benzo [α] anthracene (BaA), benzo [β]-fluoranthene (BbF), chrysene (CHR), benzo [k] fluoranthene (BkF), indeno [1,2,3-cd] pyrene (IND), dibenzo [ah] anthracene (DahA) and BghiP (Kargar-Shouroki et al., 2021).The presence of PAHs has been linked to bitumen's potential carcinogenicity, and the International Agency for Research on Cancer (IARC) classified occupational exposure to asphalt and its emissions during road paving as possibly carcinogenic to humans (Group 2B), owing primarily to its PAHs content (IARC,2013; Xu et al., 2018).

In the asphalt plants, liquid asphalt was mixed with crushed rock, gravel, and sand (collectively called aggregates) to make pavement, which was used for road construction. Asphalt workers are exposed to different hazardous substances, including PAHs emitted from hot mix asphalt as well as during pavement jobs. Therefore, exposure to asphalt became a major risk factor in the field of occupational and environmental perspective views. Adverse health effects among asphalt workers caused by irritative symptoms in the eyes and upper airways ( Raulf-Heimsoth et al., 2007), reduced lung function, increased mortality due to obstructive lung diseases (Olsen et al., 2021), an increased risk of lung and bladder cancer as well as heart diseases(Mundt et al., 2018; Olsson et al., 2010). Epidemiologic studies also revealed increased lung, skin, and bladder cancer risks for employees exposed to PAHs as well as for residents of urban and nearby neighbourhoods ( Olsson et al., 2010; Boada et al., 2015; Petit et al., 2019; Mundt et al., 2018; Shabbaj et al., 2018; Noroozi et al., 2021).

This issue raises awareness and captures the attention of the health of workers involved in the asphalt-associated industries in India. There is a lack of nationally information among asphalt workers about the nature of PAHs exposure and also limited data on exposures at a population level elsewhere in this sub-continent. This study will help inform efforts to control or prevent occupational exposure to PAHs in the asphalt paving workplace. Therefore, the aim of this study was to investigate and compare personal exposure to airborne PAHs exposure levels at hot mix plant and during paving in field experiments in real working environments.

Study Population

A total of 91 workers comprising the two job categories, i.e., 54 asphalt hot mixing plant workers and 37 road paving workers, participated in this study. The hot mix plant workers include those who undertake the job of transferring hot bitumen into the silo, which comes through the tankers, and those who do the job of mixing the stone, gravel into a rotating drum or mixer, which finally goes into the conveyor belt for transferring to asphalting locations. The paving workers are those who apply hot-mix asphalt while resurfacing the roads. The majority of these workers generally migrate from rural areas to urban cities in search of work. Informed consents were obtained from each study participant prior to sampling after explaining the objective of the study to both the occupier of the plant and the worker.

Personal Air Sampling

Personal air samples (both vapour and particulate phases) were collected from each worker in accordance with NIOSH Method 5506 (NIOSH, 1998) among the hot asphalt mixing plant workers who were engaged in the sections namely cabin, conveyor belt, mixer, and loading areas respectively. In paving areas, the drivers, pavers, and finisher workers were monitored. The SKC Personal Sampler is attached to a 37-mm-diameter filter (laminated PTFE of 2.0 µm pore size, Zefluor, Pall Gelman Sciences, Cat. No. P5PJ037) placed in a cassette near the worker’s breathing zone to collect particulate PAHs. The sorbent tube (XAD-2, ORBO 43, Supelco, Cat. No. 2-0258) was attached in line and downstream from each filter cassette to collect the vapour phase PAHs. The flow rate was maintained at 2.0 LPM/min, and it was checked before, during, and after sample collection using a TSI flow calibrator. Opaque filter cassettes and aluminium foil-wrapped sorbent tubes were used in the study to prevent sample degradation due to sunlight. After monitoring, the samples were transported in a cold chain to the laboratory and stored at -20°C until analysis.

Analytical Procedure for the determination PAHs

The composite samples collected from the workers on filter paper and sorbent tubes were extracted with acetonitrile and cycloxexene in an ultrasonic bath for 30 minutes at room temperature as per NIOSH Method 5506. An equal-mass aliquot of extract samples was combined for analysis. The extracts were concentrated under a rotary evaporator and changed to acetonitrile. All these concentrated samples were filtered through a syringe filter (0.45 m millipore PTFE filters) before analysis in HPLC. All the samples were analysed for a mixture of sixteen PAHs simultaneously. A mixture of sixteen PAH standards, namely Naphthalene (NAP), Acenaphthylene (ACPy), Acenaphthene (ACE), Fluorene (FLU), Phenanthrene (PHE), Anthracene (ANT), Fluoranthene (FLA), Pyrene (PYR), BaA, CHR, BbF, BkF, BaP, DahA, BghiP and IND, were considered for the current investigation. Samples (20µl) were injected using an HPLC system equipped with a fluorescence detector (FLD) and a C18 reversed phase column (250mm x 4.6 nm, 5 m). A solvent gradient was acetonitrile and deionized water, with a linear gradient from 60% acetonitrile/40% deionized water to 100% acetonitrile at 1.5 ml/min over 50 minutes. The HPLC system was calibrated using an external standard mixture. A standard mixture containing 16 PAHs provided by Sigma Aldrich was used for calibration and quantification. The excitation and emission wavelengths were 340 nm and 425 nm, respectively.

A field blank was collected for each phase of sampling, and blank correction by the crew was performed. The detection limit was determined by serially diluting known working standards and analyzing them on the instrument to a level of a signal-to-noise (S/N) ratio of three. The recovery efficiency of the method was determined by replicate analysis of a spiked known concentration of standard PAH compounds with a filter sample. Most of the compounds provided high recoveries, with mean values ranging between 75 and 90%.

Data analysis

IBM SPSS Statistics Version 21.0 was used as a statistical tool. In order to evaluate possible differences between each independent sample for each sampling place, student’s t-tests were used. Statistical analyses of data from coke oven gases were performed. In all cases, a P-value of < 0.05 was considered significant. This analysis was based on the assumption that all the samples collected represent a randomly selected and thus representative sample of the population.

Exposure Risk Assessment for Personal Exposure

A human health risk assessment is an estimate of the type and likelihood of adverse health effects in persons exposed to chemicals presently or in the future. According to the effect of chemicals on human health, this risk can be classified as either a cancer risk or a non-cancer risk. Cancer risk is viewed as a stochastic response, which means that increasing the dose does not necessarily increase the severity of the response but rather the possibility of it occurring. Non-cancer risk assessments, on the other hand, are viewed as deterministic, implying that increasing the dose will result in a more severe response (Mateos et al., 2018). Risk estimations from exposure to air pollutants via inhalation are a tool that contributes to air quality management. In this study, the inhalation exposure pathway of air particles contaminated with PAHs that can cause cancer was considered for the assessment of human health risk. We used the classification of International Agency for Research on Cancer (IARC) of WHO and identified 7 PAHs classified as carcinogenic (Group 1; BaP), probably carcinogenic (Group 2A; DahA), and possibly carcinogenic (Group 2B; BaA, Chr, BbF, BkF, and InP) to humans. Although PAHs other than these 7 PAHs possess limited carcinogenicity, those PAHs can increase the overall exposure when present in PAH mixtures (Yadav et al., 2020).

To calculate the risk of PAH compounds exposure in the workplace through inhalation, the formula of the Risk Assessment Information System toolkit (RAIS 2022) provided by The California Environmental Protection Agency was used. The tool was considered for calculating the risk value, since the workers have performed their duties in outdoor environment and inhaled PAHs from surrounding work atmosphere. In health risk assessment, a risk of 10^− 6 (when the risk of developing cancer over a human lifetime is 1 in 1,000,000) represents a negligible cancer risk; a value between 10^− 6 and 10^− 4 is defined as a potential cancer risk, and a risk that exceeds 10^− 4 (when the risk of developing cancer over a human lifetime is greater than 1 in 10,000) is a significant cancer risk (Maharjan et al., 2021).

Inhalation risk assessment for outdoor asphalt worker:

Lifetime cancer risk (LCR) is the increased probability of developing cancer as a result of a specific exposure and was calculated by multiplying the intake of a toxic substance by the cancer potency factor, as follows

Carcinogenic Air Inhalation (CDI)

\(\text{CDI }\text{out-air-}\text{inhn}\left(\frac{\text{μg}}{\text{m}\text{3}}\right)\text{=}\frac{C\text{ air} \left(\frac{\text{μg}}{\text{m}\text{3}}\right)xEF\text{out}\left(\frac{225days}{year}\right)xED\text{out}\left(25years\right)xET\text{out}\left(\frac{8hours}{day}\right)x\left(\frac{1day}{24hours}\right)}{AT\text{out}(\left(\frac{365days}{year}xLT\left(70years\right)\right)}\) -- Eq. (1)

C _air (Concentration of PAH compound in air), ED _out (Exposure duration-outdoor workers)year = 25years, ET_out (exposure time-outdoor workers) hours. EF_out (exposure frequency-out door workers) day/years = 225, LT (Life Time) years = 70

Inhalation Risk (IR) = Eq. (1) x Inhalation Unit Risk* (µg/m³)⁻¹

Risk = a unitless probability of an individual developing cancer over a lifetime; CDI = chronic daily intake or dose and Inhalation Unit Risk (IUR) proposed by California Environmental Protection Agency (CEPA)

Non-cancer chronic inhalation health impacts were assessed by a direct comparison of the average personal exposure with a substance specific inhalation reference concentration (RfC)-. The hazard quotient (HQ) of each compound was calculated:

Non-Carcinogenic Air Inhalation (CDI)

\(\text{CDI }\text{out-air-}\text{inhn}\left(\frac{\text{μg}}{\text{m}\text{3}}\right)\text{=}\frac{C\text{ air} \left(\frac{\text{μg}}{\text{m}\text{3}}\right)x\left(\frac{\text{mg}}{1000\text{μg}}\right)EF\text{out}\left(\frac{225days}{year}\right)xED\text{out}\left(25years\right)xET\text{out}\left(\frac{8hours}{day}\right)x\left(\frac{1day}{24hours}\right)}{AT\text{out-a}(\left(\frac{365days}{year}xET\text{out}\left(25years\right)\right)}\) -- Eq. (2)

Inhalation Hazard quotient (HQ) = Eq. (2) x Chronic RfC^* (mg/m³)

where HQ is the hazard quotient for each PAH compound; Eq. (2) is the modelled personal exposure to each PAH compound; and Rfc is the reference exposure limit for the compound. An HQ value of one or less indicates that adverse health effects are not expected to result from exposure to these PAHs. As the HQ increases above one, the probability of human health effects increases by an undefined amount, such that PAH compounds could be of public health concern. Cumulative non-cancer risks were assessed by summing the HQs of the PAHs that affected the same target organ system.

The present study has been focused on the personal exposure to PAHs emitted from asphalt hot mixed pant and paving to find out the amount of PAHs exposure and its potential risk among the workers. Exposure to PAHs is a significant concern because of their carcinogenic and non- carcinogenic on human health. The concentrations of total PAH (TPAHs; 16 PAH compounds) and individual PAH inhaled by workers, 37 from paving area and 54 samples from plants, have been described in Table-1. The exposure level of PAHs exposure did not exceed the set by the limit (200µg/m³) set by the Occupational Safety and Health Administration (OSHA) or limit prescribed by (ACGIH, 2017). However, total average PAHs exposure among paving workers was 38.65 ± 8.75µg/m³ which was higher comparing with the plant workers (9.03 ± 1.2275µg/m³) and it was statistically significant. Among the individual PAH compounds, concentrations of FLU, FLA, PYR, BaP and BghiP compounds were highly significant (p 0.05) among paving and other PAHs compound such as NAP, ACPy, ACP, FLU, PHE, FLA, PYR, BaA, BkF, BaP, DahA, BghiP and IND were statistically significant. On the other hand, CHR, BbF & DahA were relatively high level of exposer by the plant workers compare to paving workers.

Table 1

Time-Weighted average of PAHs (µg/m³) personal exposure among the workers’ breathing zone of the asphalt mixing plant and road paving workers
PAH Compounds	Total (N-91)			Paving(n = 37)			Plant(n = 54)
PAH Compounds	Range	Mean	SD	Range	Mean	SD	Range	Mean	SD	P (Paving vs Plant)
NAP	ND-12.41	0.77	1.56	ND-12.41	0.86	2.1	ND-6.26	0.7	1.06	0.627
ACPy	ND-7.95	0.43	1.23	ND-7.95	0.61	1.63	ND-4.51	0.31	0.83	0.248
ACE	ND-35.73	1.14	4.59	ND-35.73	2.18	7.09	ND-3.30	0.43	0.62	0.075
FLU	ND-57.71	2.11	7.88	ND-57.71	4.54	11.86	ND-9.62	0.46	1.71	0.014*
PHE	ND-21.93	1.31	3.58	ND-21.93	2.19	5.42	ND-4.19	0.71	0.94	0.052
ANT	ND-1.91	0.10	0.31	ND-1.91	0.2	0.47	ND-0.33	0.03	0.05	0.009*
FLA	ND-6.55	0.31	1.11	ND-6.55	0.73	1.66	ND-0.29	0.02	0.04	0.002*
PYR	ND-0.75	0.10	0.16	ND-0.75	0.15	0.22	ND-0.52	0.07	0.1	0.014*
BaA	ND-0.49	0.06	0.08	ND-0.49	0.06	0.1	ND-0.24	0.05	0.07	0.524
CHR	ND-0.24	0.04	0.05	ND-0.17	0.03	0.04	ND-0.24	0.05	0.06	0.165
BbF	ND-8.95	0.78	1.74	ND-0.40	0.03	0.07	ND-8.95	1.3	2.12	0.000*
BkF	ND-48.62	1.94	6.07	ND-48.62	2.73	8.46	ND-25.95	1.4	3.63	0.307
BaP	ND-59.05	3.28	8.46	ND-59.05	7.45*	12.17	ND-2.98	0.43	0.7	0.000*
DahA	ND-14.29	1.21	2.48	ND-9.80	1.31	2.19	ND-14.29	1.13	2.67	0.733
BghiP	ND-79.06	7.15	17.05	ND-79.06	15.23*	24.03	ND-35.17	1.61	4.97	0.000*
IND	ND-6.28	0.34	0.88	ND-6.28	0.35	1.18	ND-2.50	0.34	0.61	0.957
TPAHs	0.02-184.71	21.07	37.36	0.02–184.70	38.65*	53.25	0.29-36.00	9.03	8.95	0.000*

ND: Not Detected; *=significant (p < 0.05; Paving vs. Plant).

In the present study, in the hot mixed plant, out of 54 workers, 6 participated in the study as cabin operators, 18 from conveyer belts, 20 from mixer plants, and 10 loaded bitumen. On the pavement site, 6 people were operating the asphalt paving equipment as drivers, 25 workers were ground manual pavers, and the remaining 6 workers were finishing jobs. Comparing the exposure level, it was found that the workers in the ground paver and finishing sections were exposed to higher levels of TPAHs and BaP (Table 2). The BaP concentration was significantly (p < 0.05) contributed to the total PAHs in the cabin, conveyers’ belt, mixer and paver section. in the It was observed in the sample collection time that these two job categories of workers were very close to asphalt material and inhaling more contaminated air while performing duties.

Table 2

Time-Weighted average exposure to PAHs (µg/m³) among the workers in different section of the asphalt mixing plant and road paving workers
Section		N	TPAH	BaP	P-Value
Section		N	Mean ± SE (µg /m³)		P-Value
Plant (N = 54)	Cabin	6	13.24 ± 3.7	0.34 ± 0.27	0.021*
	Conveyers Belt	18	6.94 ± 1.21	0.62 ± 0.21	0.001*
	Mixer	20	10.0 ± 2.25	0.20 ± 0.06	0.001*
	Loading	10	8.3 ± 3.71	0.63 ± 0.28	0.061
Paving (N = 37)	Driver	6	16.87 ± 16.19	3.39 ± 3.01	0.350
	Paver	25	41.32 ± 11.05	7.7 ± 2.62	0.002*
	Finisher	6	49.30 ± 24.03	10.49 ± 5.00	0.133

*=significant (p < 0.05)

It was observed that the level of TPAHs (0.02-184.71 µg/m³) was almost similar as found among the Norway asphalt workers (0.003-150 µg/m³)(Burstyn et al., 2002), but higher than the level observed among asphalt paver ( mean 3.21 µg/m³) in UK (Unwin et al., 2006) and 2.3µg/m³ (range 0.2–23.8 µg/m³) among Swedish road paving workers (Järvholm et al., 1999). In our study, the mean level was 21.07 µg/m³. Also the inhalation exposure range was found among the paver was 0.02–184.70 µg/m³ and higher than (2.8–43.0 µg/m³) the study carried out by McClean et al. (McClean et al., 2004) among the pavers. A recent study done in Sweden, found air bone PAHs value was 2.75 µg/m³ median value with 0.71 µg/m³ − 6.24 µg/m³ at 5%-75% percentile among 19 paving workers, which was lower exposure that present study (Xu et al. 2018b). A the same time as the results of the present study are compared with those of other European studies conducted on asphalt workers, the median levels of airborne exposure to PAH in Italy seem to be similar to those found in Norway, Sweden, and the United States (Burstyn et al., 2002); (Järvholm et al., 1999); Watts et al. 1998; (Cirla et al., 2007), but ten-fold inferior to those found in Finland (Heikkilä et al., 2002). It could be noted that the varied concentration of PAH measured in our study could be due to asphalt composition, hot mixed plant and final product temperature, wind direction and humidity. The application temperature is one of the most important factors in determining the chemical composition and concentration of asphalt fumes(Burstyn et al., 2002). The amount and composition of PAHs are distinctly influenced by changes in temperature (Clifford R. Lange and Mary Stroup-Gardiner, 2007). It was observed that binder temperatures at or below 150^◦C, only very small amounts of mostly 2- and 3-ringed PAHs were emitted. Despite the fact that various researchers established elevated temperatures increases total fume emissions in asphalt, but they do not precisely report on PAH emissions (Hansen 1991). PAH emissions from bitumen are highly temperature-dependent. Increasing concentrations of individual PAH compounds were observed with increasing binder temperature. The mean pyrene level (0.3 µg/m³) was double in paver in Greater Boston area (McClean et al., 2004) whereas our finding is 0.15µg/m³. The study in Europe (Heikkilä et al., 2002) revealed that the mean of TPAHs 2.38 µg/m³ among the plant (roller operators) and 4.28 µg/m³ in paving operators, but the mean level of PAHs was 38.65 µg/m³ in paver and 9.03 µg/m³ among the plant workers. Thus, in the both study the paver workers are exposed to higher concentration PAHs than the plant workers. It might be due closed contact with hot asphalt mixture and it leads direct exposure among the paver, but in the plant the mixing process was mechanical including tar mixing to loading. BghiP the most carcinogenic PAH and toxicity significant same as BaP considering risk factor and it was dominant in the PAH in both the site with strong correlation in the present study. The potentially toxicology of BaP and BghiP support as marker of PAHs and occupational exposure to asphalt fumes.

We observed that both the asphalt mixing plant and paving workers are exposed to both particulate and vapour phase PAHs emission in their workplace which may be detrimental to their health. During asphalting work process, dust is generated and it might cause irritation as perceived by some workers. They are not given much importance to wearing the respiratory masks while working in hazardous job operations. It was already study that airborne bitumen exposure was associated with acute respiratory symptoms (Raulf-Heimsoth et al, 2007). Wind speed is associated with exposure, which likely provided natural ventilation to the work area and reduced the potential for contact with airborne dust. It could be noted from the results that the PAHs could possibly penetrate through inhalation or dermal routes more among road paving workers than the asphalt mixing plant workers, as the concentration TPAHs is higher in road paving operations. The chronic increased exposure is capable of inducing adverse effects on such workers. The American Conference of Governmental Industrial Hygienists (ACGIH) currently recommends a threshold limit value for asphalt fumes of 0.5 mg/m³ (benzene-soluble aerosol), while the National Institute for Occupational Safety and Health (NIOSH) recommends an exposure limit of 5 mg/m3 (total particulate during any 15-minute period). The Occupational Safety and Health Administration (OSHA) currently have no standard for exposure to asphalt fumes. But in the absence of any such occupational health standards in developing countries like India, the available standards of other referred regulatory agencies could be used to recognise the hazards. This will help in the development of strategies for minimising the risk among unorganised workers of this kind.

Health Risk Assessment of Asphalt Workers Exposed to PAHs

A health risk assessment is the scientific evaluation of potential adverse health effects resulting from human exposure to a particular hazard, and the risk of pollution to health in a population is usually represented by a concentration-response function, which is typically based on Relative Risk (RR) estimates derived from epidemiological studies (González Ortiz et al., 2021). The RR estimate defined the probability of an adverse health outcome (e.g., premature death, asthma attack, emergency hospital admission, cancer, etc.) occurring in a population exposed to a higher level of air pollutant relative to that in a population with a lower exposure level. The inhalation exposure pathway of PAHs that can cause both cancer and non-cancer was considered for the assessment of human health risk. Table 3 presents the estimated lifetime excess cancer risks based on inhalation daily doses and inhalation cancer potency factors. Considering the cumulative cancer risk, BaP and DahA rank in the first category, that is, with high median cancer risk estimates greater than 1 × 10^− 5. BbF, IND, NAP and BkF rank in the second category, with medium cancer risk estimates between 1 × 10^− 6 and 1 × 10^− 5. BaA and CHR are in the lowest category, with median cancer risk estimates less than 1 × 10^− 6. All are in the ranges for which the U.S. EPA suggests taking action to reduce exposures. For all PAHs, the total cancer risks for paving workers were higher than those for workers in plants. Considering the ranking of the individual PAH compounds, the cancer risk contribution by DahA (4.98 x10^− 05) is higher among the plant workers, followed by BaP (1.91 x10^− 05). On the other hand, BaP (3.28 x10^− 04) contributes more risk among paving workers than DahA (5.78 x10^− 05). The percentage contribution of individual PAH compounds towards the estimated lifetime excess cancer risks in plant and paving workers is shown in Figs. 1a and 1b. 62.09% of risk is contributed by DahA followed 23.7% by BaP in the plant and DahA (14.8%) and BaP (83.9%) in the paving, respectively.

For non-cancer health impacts, NAP and BaP have inhalation reference concentrations. Thus, an HQ of one was exceeded for the respiratory system, which suggests potential adverse chronic health impacts at these receptor locations. A mean HQ of less than one except for BaP, indicating that only Bap concentration exceeded the chronic inhalation reference concentration. Thus, HQ of one was exceeded for the respiratory system, which suggests a potential adverse chronic health impact at the receptor location.

Table 3

The risk expression estimation value with PAHs compounds in the plant and paving areas of asphalt industries workplace with total risk value:
PAH Compounds	IUR† (µg/m³)⁻¹	Chronic RfC^* (mg/m³)	Inhalation HQ			Inhalation Risk (IR)
			Plant	Paving	Total	Plant	Paving	Total
NAP	3.40 x10^− 05	0.003	4.85x10^− 02	5.91x10^− 02	1.08x10^− 01	1.77x10^− 06	2.15x10^− 06	3.92 x10^− 06
BaA	6.00 x10^− 05	-	-	-	-	2.26x10^− 07	2.75x10^− 07	5.01 x10^− 07
CHR	6.00 x10^− 07	-	-	-	-	2.07x10^− 09	1.37x10^− 09	3.44 x10^− 09
BbF	6.00 x10^− 05	-	-	-	-	5.72x10^− 06	1.46x10^− 07	5.87 x10^− 06
BkF	6.00 x10^− 06	-	-	-	-	6.15 x10^− 07	1.20 x10^− 06	1.82 x10^− 06
BaP	6.00x10^− 04	0.000002	4.45x10⁰¹	7.65x10⁰²	8.10x10⁰²	1.91 x10^− 05	3.28 x10^− 04	3.47 x10^− 04
DahA	6.00 x10^− 04	-	-	-	-	4.98 x10^− 05	5.78 x10^− 05	1.08x10^− 04
IND	6.00 x10^− 05	-	-	-	-	3.09x10^− 06	1.53x10^− 06	4.62 x10^− 06
Total Risk			4.45x10⁰¹	7.65x10⁰²	8.095x10⁰²	8.03x10^− 05	3.91x10^− 04	4.71x10^− 04
^*Rfc-inhalation reference concentration and †IUR-inhalation reference concentration, chemical-specific

The impact of PAHs on human health depends mainly on the duration, route of exposure, and amount or concentration of PAHs one is exposed to, as well as the relative toxicity of the PAHs. PAHs can be adsorbed with dust particles, and exposure to PAHs usually occurs by breathing contaminated air. PAHs generally have a low degree of acute toxicity to humans. Occupational exposures to high levels of pollutant mixtures containing PAHs have resulted in symptoms such as eye irritation, nausea, vomiting, diarrhoea and confusion. Mixtures of PAHs are also known to cause skin irritation and inflammation. ANT, BaP and NAP are direct skin irritants. But, ANT and BaP are reported to be skin sensitizers, i.e., they cause an allergic reaction in the skin of animals and humans(Abdel-Shafy & Mansour, 2016). Some studies have shown noncarcinogenic effects that are based on PAH exposure doses. Due to their non-carcinogenic properties, Person who has breathed in or comes to contact with mixtures of PAHs and PAHs-enrich chemicals for long periods of time may have health impacts. After chronic exposure, the non-carcinogenic effects of PAHs involve primarily on pulmonary, gastrointestinal, renal, and dermatologic systems. Many PAHs are only slightly mutagenic or even non-mutagenic in vitro; however, their metabolites or derivatives can be potent mutagens. The carcinogenicity of certain PAHs is well established in laboratory animals. Researchers have reported increased incidences of skin, lung, bladder, liver, and stomach cancers, as well as injection-site sarcomas, in animals. Animal studies show that certain PAHs can also affect the hematopoietic and immune systems and produce reproductive, neurologic, and developmental effects. Health risk evaluation has been considered a valuable tool, but it is difficult to attribute observed health effects to specific PAHs because most exposures are to PAH mixtures.

The purpose of this type of research study was to quantify asphalt workers exposure to PAHs during work. Monitoring PAH exposure in the workplace may play a crucial role in identifying excess exposures before substantial biological changes and health damage emerge. The results of our study demonstrate that the asphalt workers are exposed to PAHs constantly at their work sites, and inhalation represents the most significant route of chronic exposure for air containments that affect the lung and airways.

The calculated health risks values presented here are just a portion of the total exposure risk and both The calculated health risk values for asphalt workers are only a portion of the total exposure risk, with both HQ and HI levels higher than the general population (WHO recombinant level), resulting in harmful health risks. We recommend that the emissions in workplace should be controlled at the source itself; otherwise, the uptake by inhalation or skin absorption of such toxic chemicals by the workers is inevitable. It is also very difficult to restrain absorption through the skin due to the high lipophilic character of PAH, which may lead to higher absorption rates in these workers. The workers engaged in these asphalt-associated jobs do not give much importance to safety aspects due to a lack of awareness of their ill effects. The workers assume that wearing masks, gloves, safety shoes, and airtight, PAH-impermeable clothes may lead to uncomfortable work for them in their work execution. To our best knowledge, this is the first study in India to measure the airborne emissions and personal exposure measurements of asphalt mixing plant and road paving workers. Therefore, our study could be helpful to policymakers and contractors engaging these workers for better occupational hygiene practices and stringent measures to be implemented to prevent any ill effects of these informal workers.

Acknowledgement
The authors are highly grateful to the Director, ICMR-National Institute of Occupational Health, Ahmedabad, for granting permission to conduct the study and to CAMH, Kolkata, for moral support. The skilled technical assistance provided by ROHC (S) staff is acknowledged. Assistance rendered by asphalt plant owners at Bangaluru, India, was gratefully acknowledged.

Ethics approval and consent to participate:

The approval was obtained from the Institute Ethics Committee of the ICMR-Regional Occupational Health Centre (Southern), Bangaluru. All the participants were provided with the details of the study and its objectives in their local language. An informed consent form was circulated to them for better understanding, and they were allowed to voluntarily withdraw if they were not interested in the study. The data obtained is archived in the Institute Ethics Committee document division as per standard procedures, and the confidentiality of each participant is maintained.

Competing interest:

The data obtained is archived in the Institute Ethics Committee document division as per standard procedures, and the confidentiality of each participant is maintained and if you demand them, we will send the file to you.

Funding:

No funding was obtained for this study

Authors Contribution:

B. Ravichandran has designed the study proposal, data analysis, and interpretation. Somnath Sen has supervised the completion of the study, including personal monitoring with his team, collection of data, analysis of samples, interpretation, and drafting the article. V Dhananjayan has collected the data, checked the accuracy of the data, drafted the article, and done a critical revision of the article, and J Narayana has alsoconceptualised the proposal and done a critical revision of the article. All four authors have final approval of the version to be published.

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No competing interests reported.

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Personal exposure to polyaromatic hydrocarbon and inhalation risk assessment among asphalt hot mixed plant and road paving workers

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Abstract

Figures

Introduction

Material and Methods

Study Population

Personal Air Sampling

Analytical Procedure for the determination PAHs

Data analysis

Exposure Risk Assessment for Personal Exposure

Inhalation risk assessment for outdoor asphalt worker:

Carcinogenic Air Inhalation (CDI)

Non-Carcinogenic Air Inhalation (CDI)

Results and Discussion

Health Risk Assessment of Asphalt Workers Exposed to PAHs

Conclusion

Declarations

References

Additional Declarations

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