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Aerosol Science and Engineering

, Volume 2, Issue 4, pp 173–181 | Cite as

Polyaromatic Hydrocarbons Depositions and Their Carcinogenic Risk Assessment in the Foundry Workers

  • Somnath Sen
  • Jogattappa Narayana
  • Beerappa Ravichandran
  • Venugopal Dhananjayan
Original Paper
  • 231 Downloads

Abstract

The study was initiated to determinants of inhalation exposure to polycyclic aromatic hydrocarbon compounds (PAHs) among iron foundry workers in different workplace namely, molding, melting, shaking, blasting and finishing sections. The study population included five sections of foundry workers: 22 molding, 25 melting, 20 shaking, 18 blasting and 15 finishing workers. During work shifts, personal air samples were collected from each worker’s breathing zone using a PTFE filter and cassette holder connected in series with an XAD-2 sorbent tube. The entire sample were analysed for sixteen PAHs with HPLC. The total inhalation exposure of total PAHs (ΣPAHs) concentrations was 46.64 μg/m3 ranging 0.08–478.43 μg/m3 in all the samples. The PAHs with lower molecular weight and higher molecular weight contributed 55.02% and 44.98%, respectively, to the ΣPAHs. About 16% exposure samples collected at various sections of foundry exceeded the PAHs level prescribed by NIOSH standard limit. The highest level of ΣPAHs were found in the molding (82.64 μg/m3) followed by finishing (67.86 μg/m3), blasting (34.74 μg/m3), shaking (25.04 μg/m3) and melting (23.48 μg/m3) sections, respectively. By applying risk assessment it was estimated that the total unit risk of PAHs harming the foundry workers was 9.43 × 10–4 and about 95% of total risk is contributed by benzo[α]pyrene (BaP) and dibenzo [α h]anthracene (DahA). The study indicating the inhalation risk due to these PAHs exposures are not negligible and should be taken into account for health protection of the workers to address the quantitative aspects relating lung cancer risks to PAHs compounds in foundries.

Keywords

Foundry PAHs Inhalation Risk Assessment 

1 Introduction

The complexity of the raw material, i.e., scrap with different additives used in the foundry process and emission of chemicals in different units makes it difficult to identify the specific component(s) responsible for adverse health effects of the workers. Known different toxic pollutants have been found in foundry aerosol generated at worksites (Oliver et al. 2005). Observations of acute health effect from airborne aerosols and the potential for chronic health effects, including cancer, warrant continued diligence in the control. The frequent detection of silica or other mineral dust, metal fumes and dust content in the worksites have been reported, but data are limited concerning the personal exposure of carcinogenic PAHs compounds generated at foundry worksite. The sources of PAHs are binding agents (tar, coal and other organic chemicals that polymerise), pyrolysis products and oil mist in rolling mill operations (Gaertner and Theriault 2002). Moreover, PAHs in both phases (vapour and particulate) generated at high temperatures are probably more likely to carcinogenic PAHs than generated at lower temperatures. It was also reported that the total exposure burden of PAHs was highest in the workplace (Brandt and Watson 2003; Hansen et al. 2008). Among various PAHs, the particulate PAHs are considered to be significant hazardous substances to human health through breathing, of which the fine particulate fraction of PAHs absorbed through respiratory tract and gets accumulated in different parts of the human body (Zhang et al. 2012). Studies on human being show that PAHs exposed through respiratory or dermal contact for long periods can also develop cancer (Armstrong et al. 1994; Pliskova et al. 2005). Exposure to PAHs was also associated with mainly for an increased risk of lung, laryngeal, skin, kidney and urinary bladder cancer (ATSDR 2013). It could interfere with cell membrane function and the coupled enzyme system, and metabolites of PAHs may bind to DNA which can cause chemicals disruption and cell damage (Nisbet and Lagoy 1992). BaP is the most studied PAH, and other PAHs have been ranked according to cancer potency (Ramírez et al. 2011). In addition to their carcinogenic properties, PAHs are known as cytotoxic (Rogers et al. 2002; Yuan et al. 2010). On the basis of available human and animal evidence, The US Environmental Agency has listed 16 typical PAHs (Yan et al. 2004) as priority chemical because their toxicity and carcinogenic effect (Yan et al. 2004). These 16 PAHs classified into four group as follows-Group 1: carcinogenic to humans, Group 2A: probably carcinogenic to humans or Group 2B: possibly carcinogenic to humans by IARC (1983). Risk associated with PAHs in the workplace and estimation of lifetime lung cancer risk study was a recent focus (Zhang et al. 2012) because it is presumed that carcinogens present in human lungs contribute to the incidence of lung cancer and most of the carcinogens are inhaled with particulate matter via the respiratory tract into the lung alveoli. PAHs like benz[a]anthracene (BaA), BaP, benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), chrysene (CHR), DahA, and Indeno(1,2,3-cd) pyrene(IND) considered as possible carcinogens (Menzie et al. 1992) and Benzo(a)pyrene has been identified as most significant carcinogenic compound (Kuo et al. 1998; Wang et al. 2002) and is often used as indicator of cancer risk for target population. Toxicity equivalency factor were recommended for calculating the relative toxicity of individual PAH to BaP for the purpose of simplifying risk assessment (Tseng et al. 2014).

In this present study the personal sampling was conducted to collect air-bound PAHs at different sections (molding, melting, shaking, blasting and finishing) of the foundry to investigate PAHs level at the workplace to know the distribution of PAHs compounds for estimating the lifetime lung cancer risk of occupational exposure to PAHs.

2 Materials and Methods

2.1 Study Area

The study was conducted in the iron and steel foundries located in Shimoga in Karnataka and Coimbatore in Tamil Nadu, India, during 2015–2016. The study was planned after a preliminary walk-through survey in all the plants. Personal monitoring was carried out in various locations such as molding, melting/furnace, shaking, blasting and finishing sections of the workplace in the day shift (i.e., 8:00 a.m. to 4:30 p.m. excluding a half-hour break). These foundries were operating in the day shift only. The study population included five sections of foundry workers: 22 molding, 25 melting, 20 shaking, 18 blasting and 15 finishing. All participants were male and a written informed consent was obtained from each study subject prior to sampling.

The potential source of PAHs is from sand mixing and fumes from pouring and shakeout section which is near to molding section. The foundry is coming under small and medium scale categories of industry and all the operation are carried out in one floor with all the process. PAHs result from thermal decomposition (melting process) of carbonaceous ingredients in foundry sand in a limited oxygen supply in the foundry precesses. Also it is partly vapourised under the extremely hot and adsorbed onto soot, fume or sand particles and spread throughout the workplace during shake-out and other dusty operations. In the shaking process, once casting iron was cooled while continuing to give off fugitive emissions and castings underwent further cleaning by automated shot blasting followed by an automated coarse, dry grinding to remove unwanted cast material in the finishing section.

2.2 Personal Air Sampling

Personal air samples were collected from each worker in accordance with NIOSH Method 5506 (NIOSH 1998) for 8 h. The air sampling system consisted of a Teflon filter and cassette holder to collect particulate PAHs and XAD-2 sorbent tube to collect both forms of PAHs, because low molecular weight PAHs (two- and three-ring) occur in the atmosphere during the vapour phase, whereas multi-ringed PAHs (five-ring) are bound to particles. Intermediate molecular weight PAHs (four-rings) are partitioned between the vapour and particulate phases, depending on atmospheric temperature (Srogi 2007). Personal air sampling pumps were operating at 2 l/min. The 37 mm diameter filter (PTFE-laminated with 2 µm pore size (Zefluor, Pall Gelman Sciences, and Cat. No. P5PJ037)) were placed in a cassette and attached to each worker’s lapel near the breathing zone, and the sorbent tube containing XAD-2 (ORBO 43, Supelco and Cat. No. 2-0258) was attached inline and downstream from each filter cassette. Flow rates were checked before, during and after sample collection using a digital flow meter (TSI, USA). Opaque filter cassettes and foil-wrapped sorbent tubes were used to prevent sample degradation from sunlight. Samples were transported in coolers and stored at −20 °C.

2.3 Processing of Samples and PAHs Analysis

All the samples collected on filter papers and sorbent tubes were extracted with HPLC grade acetonitrile (Merck, India) and cyclohexene (Merck, India) in an ultrasonic bath for 30 min at room temperature according to NIOSH Method 5506 (NIOSH 1998). The extracts were concentrated under rotary evaporator (Model: Syncore, Buchi,) and changed to acetonitrile. The concentrated samples were filtered through syringe filter (0.45 µm Millipore PTFE filters) before analysis in HPLC. All the samples were analysed for a mixture of 16 PAHs simultaneously. A mixture of 16 PAHs, namely, Naphthalene (NAP), Acenaphthylene (ACPy), Acenaphthene (ACE), Fluorene (FLU), Phenanthrene (PHE), Anthracene (ANT), Fluoranthene (FLA), Pyrene (PYR), Benzo(α)anthracene (BaA), Chrysene (CHR), Benzo[b]fluoranthene (BbF), Benzo[k]fluoranthene (BkF), Benzo[α]Pyrene (BaP), Dibenzo[α h]anthracene (DahA), Benzo[ghi]perylene (BghiP) and Indeno(1,2,3-cd)pyrene (IND) were considered for the current investigation. Samples (20 µl) were injected into the HPLC system equipped with the fluorescence detector (FLD) with a C18 reversed phase column (250 mm × 4.6 mm, 5 µm). A solvent gradient was acetonitrile and deionized water with linear gradient from 60% acetonitrile/40% deionized water to 100% acetonitrile at 1.5 ml/min over 50 min. The HPLC system was calibrated for quantification of PAHs using an external standard mixture containing 16 PAHs provided by Sigma-Aldrich, USA. The excitation and emission wavelengths were set at 340 and 425 nm, respectively.

A field blank was collected for each phase of sampling and blank correction by 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 3. Recovery efficiency of the method was determined by replicate analysis of a spiked known concentration of standard PAH compounds with filters sample. Most of the compounds provided high recoveries with mean values ranging between 75 and 90%. Also internally prepared standard samples were run after every eight to ten unknown samples.

2.4 Risk Assessment

To calculate the risk of PAHs compounds exposure in the indoor workplace through inhalation, formula of Risk Assessment Information System toolkit (RAIS 2013) 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 indoor environment and inhaled the PAHs from surrounding work atmosphere.

2.4.1 Carcinogenic Air Equation

Inhalation Ambient Carcinogenic (CDI) Equation (RAIS 2013):
$${\text{CDI}}_{\text{iw-air-ca}}\left( {\frac{{\upmu{\text{ g}}}}{{{\text{m}}^{3} }}} \right) = \frac{{C_{\text{air}} \left( {\frac{{\upmu{\text{g}}}}{{{\text{m}}^{3} }}} \right) \times EF_{\text{iw}} \left( {\frac{{250\;{\text{days}}}}{\text{year}}} \right) \times {\text{ED}}_{\text{iw}} \left( {25\;{\text{years}}} \right) \times ET_{\text{iw}} \left( {\frac{{8\;{\text{hours}}}}{\text{day}}} \right) \times \left( {\frac{{1\;{\text{day}}}}{{24\;{\text{hours}}}}} \right)}}{{AT_{\text{iw}} \left( {\frac{{365\;{\text{days}}}}{\text{year}} \times {\text{LT }}(70\;{\text{years}})} \right)}},$$
where Cair-Concentration of PAH compounds; EFiw (exposure frequency—indoor worker) day/year-250; EDiw (exposure duration—indoor worker) year-25; ETiw (exposure time—indoor worker) hour-8; ATiw (averaging time—indoor worker)-365; LT (lifetime) year-70.

2.4.2 The Mathematical Expression to Determine the Inhalation Ambient Air Risk is Provided Below

The equation determines the inhalation ambient Air Risk (IAAR):
$${\text{IAAR Value}} = {\text{CDI}_{\text{iw-air-ca}}} \left( \upmu{{\text{ g}}/{\text{m}}^{ 3} } \right) \times {\text{Inhalation Unit Risk}}* \, \left(\upmu {{\text{g}}/{\text{m}}^{ 3} } \right)^{ - 1}$$

*Inhalation Unit Risk (IUR) proposed by California Environmental Protection Agency (CEPA).

3 Results and Discussion

The mean concentration of PAHs exposure among workers of various sections of foundries is given in Table 1. The percentage contributions of individual PAHs to the total PAHs are illustrated in Fig. 1. The mean ΣPAHs concentrations was 46.64 ± 7.8 µg/m3 a with range of 0.08–478.43 µg/m3 in the foundries. All the 16 PAHs compounds detected were classified into two categories: low molecular weight (LM-PAHs containing two- to three-ringed PAHs), and high molecular weight (HM-PAHs, containing four- to six-ringed PAHs.
Table 1

Mean ± SE of PAHs concentration in the workplace of foundry and their contribution in total PAHs

PAH compounds

Molecular weight

Molecular formula

No. of rings

Mean ± SE (µg/m3)

% of total PAHs

Lower molecular weight

NAP

128.18

C10H8

2

5.88 ± 1.33

12.62

ACPy

152.2

C12H8

3

4.02 ± 1.16

8.62

ACE

154.2

C12H10

3

8.76 ± 2.55

18.77

FLU

166.23

C13H10

3

3.45 ± 1.76

7.39

PHE

178.24

C14H10

3

3.28 ± 1.32

7.03

ANT

178.24

C14H10

3

0.27 ± 0.07

0.58

Total (2–3 rings)

 

2–3

25.66 ± 5.74

55.02

Higher molecular weight

FLA

202.26

C16H10

4

1.00 ± 0.21

2.15

PYR

202.06

C16H10

4

1.48 ± 0.38

3.18

BaA

228.3

C18H12

4

1.63 ± 0.59

3.51

CHR

228.3

C18H12

4

1.21 ± 0.46

2.60

BbF

252.32

C20H12

5

0.28 ± 0.09

0.59

BkF

252.32

C20H12

5

0.64 ± 0.35

1.37

BaP

252.32

C20H12

5

7.20 ± 1.11

15.60

DahA

278.35

C22H14

5

2.54 ± 1.02

5.46

BghiP

276.34

C22H12

6

3.96 ± 0.74

8.49

IND

276.34

C22H12

6

0.96 ± 0.30

2.05

Total (4–6 rings)

 

4–6

20.98 ± 2.92

44.98

∑PAHs

 

2–6

46.64 ± 7.8

100

Fig. 1

The percentage of contribution of individual PAHs in total load PAHs

Among various PAHs detected, the most abundant PAHs were ACE (8.76 µg/m3), BaP (7.20 µg/m3), NAP (5.88 µg/m3) and ACPy (4.02 µg/m3). Comparatively LM-PAHs with high vapour pressure such as NAP, ACPy, ACE, FLU, PHE and ANT contributed 55.02% (mean 25.66 ± 5.74) to the ΣPAHs than the HM-PAHs which contribute only 44.98% (mean 20.98 ± 2.92) to ΣPAHs. But the HM-PAHs are carcinogenic or probably carcinogenic to human and defined as toxic compounds. Among ΣPAHs monitored for personal exposure, 16% of the personal air samples exceeded the value of 100 µg/m3 prescribed by NIOSH workplace exposure for 8 h TWA.

The personal exposures of various PAH compounds in the different shop floors are shown in Table 2. The higher mean concentration of ∑PAHs and total carcinogenic PAHs (cPAHs: BaA, CHR, BbF, BkF, BaP, DahA, BghiP and IND) were 82.64 µg/m3 and 27.74 µg/m3 in the molding section respectively, compared to other sections. The personal exposure of average BaP was high in the blasting section. The exposure loads of ΣPAHs in the finishing section were 67.86 µg/m3 followed by blasting (34.74 µg/m3), shaking sections (25.04 µg/m3) and melting (23.48 µg/m3).
Table 2

Mean concentrations of PAH compounds (µg/m3) in the personnel-exposed samples in different sections of the foundry

PAH compounds

Sections

Molding (N = 22)

Melting (N = 25)

Shaking (N = 20)

Blasting (N = 18)

Finishing (N = 15)

NAP

12.76

2.85

2.48

0.87

10.51

ACPy

9.83

2.11

0.96

0.52

6.23

ACE

21.21

4.46

1.70

1.15

14.72

FLU

1.92

6.27

0.48

4.41

1.70

PHE

3.94

0.25

6.80

3.45

2.38

ANT

0.64

0.16

0.07

0.06

0.39

FLA

1.95

0.47

0.37

0.19

2.19

PYR

2.66

0.66

0.55

0.39

3.46

BaA

2.18

0.23

0.21

0.16

6.79

CHR

3.30

0.21

0.17

0.28

2.26

BbF

0.74

0.14

0.07

0.28

0.04

BkF

0.10

1.39

0.05

0.68

0.46

BaP

5.20

1.95

8.74

15.59

6.65

DahA

9.45

0.70

0.95

0.04

0.39

BghiP

6.19

1.21

0.89

6.08

6.40

IND

0.57

0.42

0.53

0.57

3.53

Sum of eight carcinogenic PAH compounds (cPAHs)a

27.74

7.44

11.62

23.68

26.29

∑PAHsb

82.64

23.48

25.04

34.74

67.86

abenzo(a)anthracene, chrysene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(α)pyrene, dibenzo(a,h)anthracene, indeno(1,2,3-cd)pyrene and benzo(g,h,i)perylene

bNaphthalene, Acenaphthylene, Acenaphthene, Fluorene, Phenanthrene, Anthracene, Fluoranthene, Pyrene, Benzo(α)anthracene, Chrysene, Benzo[b]fluoranthene, Benzo[k]fluoranthene, Benzo[α]Pyrene, Dibenzo[α h]anthracene, Benzo[ghi]perylene and Indeno(1,2,3-cd)pyrene

The primary objective of this exposure assessment was to determinants of inhalation PAHs exposure among foundry workers. There were few studies were carried out in core area of the foundry workplace on PAHs. The findings of our study were compared with the studies conducted elsewhere. PAHs concentration in personal air samples collected among workers employed in various process in the Danish iron foundry was 9. 6–11.2 µg/m3 (Hansen et al. 1994). However, in the present study the levels were ranged between 0.08–478.43 µg/m3. The maximum ∑PAHs level (478.43 µg/m3) recorded in the present study was nine fold higher than the total PAH concentrations (52 µg/m3) reported in iron foundries at Ontario, California (Verma et al. 1982) and BaP level (45.37 µg/m3) was also 40-fold higher than the level reported in the personal air samples of Canadian foundry workers (Gibson et al. 1977). Present study level of total PAHs observed in the workplace was two–fourfold higher than the level recorded in a UK foundry (site 19) (Unwin et al. 2006) and in German (Knecht et al. 1986). Differences in operational process, climate and shop flower designs, ventilation may also be the factors for observing differences. The study carried out in Taiwan by Chen (2011) showed the mean level of PAHs in the painting area (associated with molding activity) and in melting area were 95.51 and 18.42 µg/m3 respectively which were almost equal to the present study (molding 82.64 µg/m3 and melting 23.48 µg/m3 respectively) levels.

To further extend the personal exposure of foundry workers to PAHs in the workplace, their exposure levels were compared with those of other worker place including coke plants, aluminium mfg., pot room, broiled food, traffic policemen, food stall, tar distillation, pipeline coating and wrap, timber impregnation, carbon black manufacturing industry, foundry, production of graphite electrodes, rubber products, road construction workers and highway toll stations (Lewtas et al. 1997; Kalina et al. 1998; Tjoe Ny et al. 1993; Carstensen et al. 1999; Brandt and Watson 2003; Kuo et al. 2006; Unwin et al. 2006; Hu et al. 2007; Zhao et al. 2011; Zuzana et al. 2016).

The concentrations of personal exposure of total PAHs, carcinogenic PAHs and BaP in various workplace environments were listed in Table 3. The total PAHs concentrations at the timber impregnation plant, tar distillation and pipeline coating and wrap industries were higher than other occupational workplace. The present study  found greater concentration of cPAHs compared to other studies except a study by Tjoe Ny et al. (1993) in aluminium manufacturing plant. However, the BaP concentrations in the present were concordant with the earlier study reports.
Table 3

Concentration of PAHs (µg/m3) exposures in different occupational workplaces across the world

Occupational workplace

Total PAHs

cPAHs

BaP

References

Mean

Range

Mean

Range

Mean

Range

 

Coke oven

0.005–200

4.5

0.13–200

0.006–42

Lewtas et al. (1997)

Coke oven

0.6–547

0.002–50.14

Kalina et al. (1998)

Aluminium mfg.

140

14

0.9–48

Tjoe Ny et al. (1993)

Pot room

0.01-270

0.02–23.5

Carstensen et al. (1999)

Coke oven

15.4

0.1–547

3.3

0.002–90

Brandt and Watson (2003)

Aluminium mfg.

12

1–153

4.4

0.02–24

Broiled food vendor

0.61–8.68

0.51–31.0

0.13–2.45

0.02–0.13

Kuo et al. (2006)

Coke oven

79.17

8.80–184.55

16.36

1.17–35.93

2.14

0.13–6.21

Unwin et al. (2006)

Tar distillation

278.82

51.9–1130.2

0.73

0.11–4.54

0.06

0.01–0.32

Aluminium (green carbon)

60.88

10.45–138.38

0.31

0.01–0.85

0.03

0.03–0.10

Pipeline coating and wrap

263.64

73.34–758.22

3.78

0.4–18.30

0.32

0.04–1.65

Timber impregnation

835.06

29.93–1912.6

0.05

0.01–0.11

0.01

0.01–0.011

Carbon black

10.70

1.98–69.09

0.52

0.03–4.49

0.05

0.01–0.41

Foundry

65.75

26.97–120.13

0.21

0.03–0.33

0.02

0.01–0.05

Traffic policemen

0.86

0.026

Hu et al. (2007)

Food stall

44.16–234

0.03–0.07

Zhao et al. (2011)

Aluminium production plant

55.15

0.05–777.73

0.19

0.01–2.00

Zuzana et al. (2016)

Production of graphite electrodes

54.25

0.15–147.50

1.31

0.01–3.18

Rubber products

25.11

0.23–87.50

0.63

0.02–2.27

Road construction workers

1.93

0.16–5.60

0.10

0.01–0.28

Foundry workers

46.64

0.08–478.4

20.98

0.05–114.4

7.20

0.01–45.1

This study

4 Health Risk Assessment of Foundry Workers Exposed to PAHs

Health risk assessments were carried out by inhalation PAHs exposure data in order to quantify lung cancer risk, regarding the lung cancer risk via the inhalation route. The average of 16 PAHs and BaP was 46.64 and 7.20 µg/m3, respectively. Though the lower molecular PAHs (2–3 rings) were in higher percentage than 4–6 rings PAHs, it should be noted that high molecular weight PAHs often result in more carcinogenic effect (Law et al. 2002). BaP has been widely investigated for its health effects and is regarded as the most likely carcinogenic in PAHs group. Recent studies have indicated BaP can be a better indicator than total PAHs content on characterizing the carcinogenic potency of PAHs (Petry et al. 1996; Zhang et al. 2011a, b), the unit risk suggested by Petry et al. (1996) was used in this study. Based on a data bank provided by an epidemiological study conducted by Carol et al. (1976), BaP was considered as referral unit risk and other PAH compounds’ risk was ranked according to cancer potency relative to BaP. It was suggested the unit risk of 7.0 × 10−5 (mg/m3) −1 for a 25 year occupational PAHs exposure corresponded with the averaged BaP concentration of 1 mg/m3 (Tsai et al. 2001). Therefore, it has been adopted by a recent study for assessing the lung cancer risks of general adult’s exposure to the ambient atmospheric PAHs (Tsai et al. 2001; Lin et al. 2008: Zhang et al. 2011a, b). However, for PAHs exposure the US Environmental Protection Administration suggested a different risk of 6.4 × 10−7 (mg/m3) − 1 by using the same data bank based on its total PAHs content (USEPA 1984). Based on the possible health effect of ubiquitous PAHs, inhalation unit risk proposed by CEPA were applied to estimate the risk of various PAH compounds. The value were NAP-3.4 × 10−5, BaA-0.00011, CHR-1.1 × 10−5, BbF-0.00011, BkF-0.00011, BaP-0.0011, DahA-0.0012 and IND-0.00011 respectively and cancer risk for a 70 years lifetime exposure can be estimated.

The inhalation ambient air risk associated with occupational exposure to PAHs in the foundry was shown in the Table 4. The total unit risk of PAHs in this occupational exposure group was 9.43 × 10−4 with Bap (6.46 × 10−4) and DahA (2.49 × 10−4) contributing 95% of total risk. According to the World Health Organization (2000) Air Quality Guidelines for Europe, the unit risk was 10−5 (one extra cancer case in 100,000 exposed individuals in the general population) and USEPA guideline was 10−6 (USEPA 1984). In the present study the estimated lifetime cancer risk value was 9.43 × 10−4 (9.4 people may develop cancer risk among 10,000 people exposed in the foundry). Ramírez et al. (2011) estimated an average lifetime lung cancer risk of total PAHs as 1.2 × 10−04 (1.2 additional cases per 10,000 people exposed) in the industrial area of southern Europe. The present study showed a higher risk of PAHs among foundry workers may be due to their continuous exposure adjacent to the source. In the foundry environment the PAHs emission retention time is much higher due to close environment whereas in ambient environment the dilution of air reduces to less retention time.
Table 4

The risk expression estimation value with PAH compounds in different locations of the foundry with total risk value

PAH compounds

IUR* (µg/m3)−1

Chronic RfC (mg/m3)**

Inhalation ambient air risk

Molding

Melting

Shaking

Blasting

Finishing

Total foundry

NAP

3.4 × 10−5

0.003

3.54 × 10−5

7.90 × 10−6

6.9 × 10−6

2.4 × 10−6

2.91 × 10−5

1.63 × 10−5

BaA

0.00011

1.96 × 10−5

2.06 × 10−6

1.9 × 10−6

1.4 × 10−6

6.09 × 10−5

1.46 × 10−5

CHR

1.1 × 10−5

2.96 × 10−6

1.88 × 10−7

1.5 × 10−7

2.5 × 10−7

2.03 × 10−6

1.09 × 10−6

BbF

0.00011

6.64 × 10−6

1.26 × 10−6

6.3 × 10−7

2.5 × 10−6

3.59 × 10−7

2.51 × 10−6

BkF

0.00011

8.97 × 10−7

1.25 × 10−5

4.5 × 10−7

6.1 × 10−6

4.13 × 10−6

5.74 × 10−6

BaP

0.0011

4.66 × 10−4

1.75 × 10−4

7.8 × 10−3

1.4 × 10−3

3.59 × 10−7

6.46 × 10−4

DahA

0.0012

9.25 × 10−4

6.85 × 10−5

9.3 × 10−5

3.9 × 10−6

3.82 × 10−5

2.49 × 10−4

IND

0.00011

5.11 × 10−6

3.77 × 10−6

4.8 × 10−6

5.1 × 10−6

3.17 × 10−5

8.61 × 10−6

Total risk

  

1.46 × 10−3

2.71 × 10−4

8.92 × 10−4

1.42 × 10−3

7.63 × 10−4

9.43 × 10−4

*IUR inhalation unit risk

**RfC inhalation reference concentration

Figure 2 show the inhalation lifetime lung cancer risk as per job categories of different sections of the foundry. It indicates that the molding and blasting sections the workers are at higher risk than other sections. The high concentration and inhalation unit risk value of BaP and DahA in the molding and blasting sections increased the risk factors in these sections compared to others.
Fig. 2

Inhalation lifetime lung cancer risk in different sections of the foundry

5 Conclusion

The goal of this type of research study was to quantify the workplace risk exposure to PAHs among the foundry workers. The monitoring of exposures to PAHs in the workplace may play an important role in detecting excessive exposures before the occurrence of significant biological disturbances and health impairment. In addition, there is big lack of information on human exposure to the individual PAH compound in factory workers. Risk estimation showed that the BaP and DahA compounds had a major contribution to the total risk. The average estimated lifetime lung cancer risk in the present study area was higher than the WHO and the USEPA recommended values. Despite uncertainties associated with the other co-pollutants and quantitative risk assessment calculations, the present study suggested that the inhalation cancer risk due to these PAHs exposures is not negligible and should be taken into account for health protection in the future. Therefore, specifically designed epidemiological studies are required to address the quantitative aspects relating to risks associated with BaP or PAHs exposure in the workplace atmosphere. In the intervening time to reduce the exposure, implementation of various control measures can be adopted. Effective control measures are therefore suggested to minimize exposure to such PAH emissions and other co-pollutants. Education, training and communication in all aspect of health and safety of workers need to be ascertained. Unless there is no alternative for not releasing toxic chemicals, engineering controls are the most effective way of reducing exposure. Finally, during exposure, the wearing of respirator masks fitted with activated charcoal can remove the volatile as well as particulate-bound PAHs.

Notes

Acknowledgements

The authors are highly grateful to The Director, National Institute of Occupational Health for granting permission to conduct the study. Assistance rendered by staffs of ROHC(S) is gratefully acknowledged. The authors also acknowledge the management and workers of the industry for participation in this study.

Compliance with ethical standards

Conflict of interest

On behalf of all authors, the corresponding author state that there is no conflict of interest.

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Copyright information

© Institute of Earth Environment, Chinese Academy Sciences 2018

Authors and Affiliations

  1. 1.Division of Industrial Hygiene and ToxicologyRegional Occupational Health Center (Southern)BangaloreIndia
  2. 2.Department of Environmental ScienceKuvempu UniversityShimogaIndia

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